Skip to main content

Main menu

  • Home
  • About the Journal
    • General Information
    • Scope
    • Editorial Board
    • Benefits of Publishing
    • Impact & Metrics
    • Advertising/Sponsorship
    • About the Biochemical Society
  • Current Issue
  • For Authors
    • Submit Your Paper
    • Submission Guidelines
    • Editorial Policy
    • Open Access Policy
    • Rights and Permissions
    • Biochemical Society Member Benefits
  • For Librarians
    • Open Access Policy
    • Terms and Conditions
      • Biochemical Journal- Terms and Conditions of Usage
      • Bioscience Reports- Terms and Conditions of Usage
  • For Readers
    • Rights and Permissions
    • Biochemical Society Member Benefits
  • Collections
  • Help
    • Technical Support
    • Contact Us
  • Other Publications
    • Biochemical Journal
    • Clinical Science
    • Bioscience Reports
    • Neuronal Signaling
    • Biochemical Society Transactions
    • Essays in Biochemistry
    • Emerging Topics in Life Sciences
    • Biochemical Society Symposia
    • Cell Signalling Biology
    • Glossary of Biochemistry and Molecular Biology
    • The Biochemist
    • Biochemical Society

User menu

  • Log-in
  • Subscribe
  • Contact Us

Search

  • Advanced search
  • Other Publications
    • Biochemical Journal
    • Clinical Science
    • Bioscience Reports
    • Neuronal Signaling
    • Biochemical Society Transactions
    • Essays in Biochemistry
    • Emerging Topics in Life Sciences
    • Biochemical Society Symposia
    • Cell Signalling Biology
    • Glossary of Biochemistry and Molecular Biology
    • The Biochemist
    • Biochemical Society

Log-in

Sign-up for alerts  
  • My Cart
Bioscience Reports
Browse Archive
Advanced Search
  • Home
  • About the Journal
    • General Information
    • Scope
    • Editorial Board
    • Benefits of Publishing
    • Impact & Metrics
    • Advertising/Sponsorship
    • About the Biochemical Society
  • Current Issue
  • For Authors
    • Submit Your Paper
    • Submission Guidelines
    • Editorial Policy
    • Open Access Policy
    • Rights and Permissions
    • Biochemical Society Member Benefits
  • For Librarians
    • Open Access Policy
    • Terms and Conditions
  • For Readers
    • Rights and Permissions
    • Biochemical Society Member Benefits
  • Collections
  • Help
    • Technical Support
    • Contact Us

Research Article

LINC00673 rs11655237 C>T confers neuroblastoma susceptibility in Chinese population

Zhuorong Zhang, Yitian Chang, Wei Jia, Jiao Zhang, Ruizhong Zhang, Jinhong Zhu, Tianyou Yang, Huimin Xia, Yan Zou, Jing He
Bioscience Reports Feb 08, 2018, 38 (1) BSR20171667; DOI: 10.1042/BSR20171667
Zhuorong Zhang
Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
Yitian Chang
College of Clinical Medicine, Jilin University, Changchun 130021, Jilin, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
Wei Jia
Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
Jiao Zhang
Department of Pediatric Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
Ruizhong Zhang
Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
Jinhong Zhu
Molecular Epidemiology Laboratory and Department of Laboratory Medicine, Harbin Medical University Cancer Hospital, Harbin 150040, Heilongjiang, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
Tianyou Yang
Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
Huimin Xia
Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
  • http://orcid.org/0000-0002-0103-1672
Yan Zou
Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
  • For correspondence: hejing198374@gmail.commonknut@126.com
Jing He
Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • View author's works on this site
  • http://orcid.org/0000-0002-1954-2892
  • For correspondence: hejing198374@gmail.commonknut@126.com
  • Article
  • Figures
  • Info & Metrics
  • Supplementary Data
  • PDF
Loading

Abstract

Neuroblastoma, which accounts for approximately 10% of all pediatric cancer-related deaths, has become a therapeutic challenge and global burden attributed to poor outcomes and mortality rates of its high-risk form. Previous genome-wide association studies (GWASs) identified the LINC00673 rs11655237 C>T polymorphism to be associated with the susceptibility of several malignant tumors. However, the association between this polymorphism and neuroblastoma susceptibility is not clear. We genotyped LINC00673 rs11655237 C>T in 393 neuroblastoma patients in comparison with 812 age-, gender-, and ethnicity-matched healthy controls. We found a significant association between the LINC00673 rs11655237 C>T polymorphism and neuroblastoma risk (TT compared with CC: adjusted odds ratio (OR) =1.80, 95% confidence interval (CI) =1.06–3.06, P=0.029; TT/CT compared with CC: adjusted OR =1.31, 95% CI =1.02–1.67, P=0.033; and T compared with C: adjusted OR =1.29, 95% CI =1.06–1.58, P=0.013). Furthermore, stratified analysis indicated that the rs11655237 T allele carriers were associated with increased neuroblastoma risk for patients with tumor originating from the adrenal gland (adjusted OR =1.51, 95% CI =1.06–2.14, P=0.021) and International Neuroblastoma Staging System (INSS) stage IV disease (adjusted OR =1.60, 95% CI =1.12–2.30, P=0.011). In conclusion, we verified that the LINC00673 rs11655237 C>T polymorphism might be associated with neuroblastoma susceptibility. Prospective studies with a large sample size and different ethnicities are needed to validate our findings.

  • LINC00673
  • neuroblastoma
  • polymorphism
  • susceptibility

Introduction

Neuroblastoma, originating from the developing sympathetic nervous system, is the most common extracranial tumor of infancy and childhood. The median age at diagnosis is approximately 18 months [1]. It is a fatal solid cancer accounting for approximately 8–10% of all childhood malignancies [1–3] and contributes to approximately 10–15% of all cancer-related deaths in children [4]. Despite intensive multimodal treatments [5], 5-year event-free survival for high-risk (approximately 50% of all cases) neuroblastoma patients remains less than 50% [6,7], and the 5-year survival rate for all neuroblastoma patients is approximately 50% [8]. Due to the rarity of neuroblastoma, strict associations are difficult to certify, and no particular environmental exposure has been involved in the development of this disease [1]. Thus, neuroblastoma remains a huge therapeutic challenge and global burden.

Previous genome-wide association studies (GWASs) of pancreatic ductal adenocarcinoma have identified a long intergenic non-coding RNA (lincRNA) LINC00673 rs11655237 C>T (also reported as G>A elsewhere) polymorphism at 17q25.1 region to be significantly associated with the risk of pancreatic cancer [9]. It was the most significant polymorphism in the LINC00673 [9]. Further studies have proven that the rs11655237 in exon 4 of LINC00673 forms a target site for miR-1231 binding, which weakens the tumor suppressing function of LINC00673 in an allele-specific manner and thus endows pancreatic cancer with susceptibility [10]. Moreover, LINC00673 has been identified to be associated with non-small-cell lung cancer (NSCLC) [11–13], gastric cancer [14], tongue squamous cell carcinoma [15], and breast cancer [16] consecutively. Together, these findings indicated that the LINC00673 rs11655237 appears to be implicated in the development of broad-spectrum tumors and also involved in cell homeostasis maintenance. However, the association between neuroblastoma susceptibility and LINC00673 rs11655237, is not yet reported.

To comprehensively evaluate and provide new insights into the impact of LINC00673 rs11655237 C>T polymorphism on neuroblastoma susceptibility, we performed a hospital-based case–control study using data from a Chinese Han population composed of 393 neuroblastoma cases and 812 age-, gender-, ethnicity-matched cancer-free controls.

Methods

Study subjects

The subjects included were described in our previous studies [17–20]. A total of 393 histopathological cases of primary neuroblastoma and 812 cancer-free controls from Guangdong province (South China) and Henan province (North China) were recruited in the current study (Supplementary Table S1). Briefly, all the 393 cases were newly confirmed and histopathologically diagnosed as neuroblastoma patients without progressive disease and previous treatments before the collection of clinical classification. The cases were genetically unrelated Chinese Han children who received treatments at the Guangzhou Women and Children’s Medical Center between February 2010 and March 2017, and at the First Affiliated Hospital of Zhengzhou University between August 2011 and April 2017. Age-, gender-, and ethnicity-matched controls were randomly recruited from children undergoing routine medical examination at the same center during the same period. The parents or guardians of the children provided written informed consent for the children’s participation in the present study. The current study was approved by the Institutional Review Board of both centers and performed in accordance with the study protocol.

Genotyping

DNA samples were extracted as previously described [21]. Briefly, DNA samples were diluted to a stock concentration of 10 ng/μl and added to 96-well plates. Genotyping for the LINC00673 rs11655237 C>T polymorphism was carried out in a 384-well plate using TaqMan Real-Time PCR method as described elsewhere [22–24]. For quality control and accuracy of genotyping results, approximately 10% of the samples were randomly selected and re-genotyped. The results were 100% concordant.

Statistical analysis

Comparison of the differences in the demographic and genotypic information between neuroblastoma cases and controls was performed by chi-square test. Hardy–Weinberg equilibrium for controls was analyzed by goodness-of-fit chi-square test. To estimate the strength of association between rs11655237 C>T polymorphism and neuroblastoma risk, unconditional univariate and multivariate logistic regression analyses were conducted and adjusted for age and gender, while odds ratios (ORs) and 95% confidence intervals (CIs) were used. Further stratified analysis was performed by age, gender, the International Neuroblastoma Staging System (INSS) clinical stages [25], and tumor sites. P-values <0.05 were considered as statistically significant. All statistical analyses were two-sided and were calculated by SAS software (version 9.1; SAS Institute, Cary, NC, U.S.A.).

Results

Demographic characteristics

The demographic characteristics of the included participants are summarized in Supplementary Table S1. No statistically significant differences were observed between neuroblastoma cases and controls regarding age (P=0.229, P=0.484, P=0.437) and gender (P=0.510, P=0.196, P=0.836) for Guangdong, Henan, and combined subjects, respectively. According to the INSS criteria, 69 (17.56%), 93 (23.66%), 68 (17.30%), 143 (36.39%), and 11 (2.80%) patients were diagnosed with clinical stages I, II, III, IV, and 4s disease, respectively. With respect to tumor sites, 153 (38.93%) neuroblastomas occurred in the adrenal glands, 87 (22.14%) in retroperitoneal regions, 109 (27.74%) in the mediastinum, and 36 (9.16%) in other regions.

LINC00673 rs11655237 C>T polymorphism and neuroblastoma susceptibility

The LINC00673 rs11655237 genotype frequencies and their association with the susceptibility of neuroblastoma are presented in Table 1. A total of 391 of the included neuroblastoma cases and all controls (812) were successfully genotyped. We found that the rs11655237 T allele carriers (CT/TT compared with CC: adjusted OR = 1.31, 95% CI = 1.02–1.67, P=0.033; and T compared with C: adjusted OR = 1.29, 95% CI = 1.06–1.58, P=0.013), especially mutated-type homozygote carriers (TT compared with CC: adjusted OR = 1.80, 95% CI = 1.06–3.06, P=0.029), were significantly associated with an increased risk of neuroblastoma when compared with wild-type homozygote carriers.

View this table:
  • View inline
  • View popup
Table 1 Genotype distributions of LINC00673 rs11655237 C>T polymorphism and neuroblastoma susceptibility

Stratified analysis

Next, the included participants were stratified by age, gender, tumor sites, and INSS stages. We further estimated the effects of the variant genotype of the rs11655237 C>T polymorphism on the neuroblastoma risk amongst the different strata (Table 2). We found that the rs11655237 CT/TT genotype carriers were significantly associated with an increased risk of a tumor originating in the adrenal gland (adjusted OR = 1.51, 95% CI = 1.06–2.14, P=0.021). Furthermore, we also found that the carriers of the CT/TT genotypes had a significantly increased risk of INSS clinical stage IV disease (adjusted OR = 1.60, 95% CI = 1.12–2.30, P=0.011) when compared with the carriers of the CC genotype.

View this table:
  • View inline
  • View popup
Table 2 Stratification analysis for the association between LINC00673 rs11655237 C>T polymorphism and neuroblastoma susceptibility for combined subjects

Discussion

In this hospital-based case–control study, we evaluated the association of the GWAS-identified LINC00673 rs11655237 C>T polymorphism with neuroblastoma susceptibility in 393 patients and 812 cancer-free controls. Our results revealed that the rs11655237 T allele significantly increased the risk of neuroblastoma. In addition, stratified analysis showed that the rs11655237 C>T polymorphism increased the risk of adrenal gland and clinical stage IV neuroblastoma. The results from the present study suggested that the rs11655237 T allele was positively associated with neuroblastoma and could confer neuroblastoma susceptibility.

Described as the largest subclass in the non-coding transcriptome in humans, lincRNAs are non-coding transcripts longer than 200 nts. In the past decade, the roles of lincRNAs in human disorders, including tumors, have attracted a lot of attention [26,27]. lincRNAs are known to play vital regulatory roles in various processes [28], including but not limited to imprinting (H19 [29] and KCNQ1OT1 [30]), metastasis (MALAT1 [31], HOTAIR [32], and COLDAIR [33]), X inactivation (XIST [34]), deregulation of the tumor suppressors [35], and pseudogene pairing (PTENP1 [36]). Therefore, aberrant expression and polymorphisms within lincRNAs have been associated with susceptibility to a range of human diseases, including cancers. Cancer-associated lincRNAs, which demonstrate developmental and tissue-specific expression properties along with aberrant regulation in various malignancies, may indicate new approaches for the diagnosis and treatment of cancer. Systematic identification of the expression patterns and characterization of lincRNAs together with their associated proteins might contribute to the development of lincRNA-targetted therapies for tumors and various human diseases.

LINC00673 is located at 17q24.3, which is a chromosome region recently documented to have a high frequency of loss of heterozygosity [37], and is associated with pancreatic cancer susceptibility in individuals of European ancestry [9]. Further studies have indicated that the LINC00673 rs11655237 variant, a germline C>T transition, can lead to a decrease in the level of LINC00673 in cells, which may trigger SRC-ERK oncogenic signaling, while attenuating STAT1-dependent anti-oncogenic signaling. Consistent with these functional discoveries, researchers have observed significantly decreased pancreatic ductal adenocarcinoma susceptibility in the rs11655237 C allele carriers when compared with the rs116552337 T allele carriers [10,38]. Intriguingly, LINC00673 has been proven to be associated with susceptibility, progression, and outcome of other malignancies as either a tumor suppressor or promoter. Shi et al. [39] found that up-regulation of LINC00673 can promote tumor proliferation through LSD1 interaction and repression of Neurocalcin δ in NSCLC, which implied LINC00673 as an oncogene in NSCLC. For the first time, Ma et al. [40] showed that LINC00673 promoted NSCLC metastasis by binding with EZH2 that resulted in epigenetic silencing of HOXA5. The latter is a tumor suppressor gene that inhibits NSCLC cell metastasis via regulating cytoskeletal remodeling. Lu et al. [11] found a similar situation in which LINC00673 regulated NSCLC proliferation, invasion, migration, and even epithelial–mesenchymal transition by sponging miR-150-5p. A study by Abdul-Rahman et al. [16] showed that LINC00673 levels were modulated by hormone signaling and inversely associated with breast cancer survival. Huang et al. [14] reported that LINC00673 was significantly up-regulated in gastric cancer. LINC00673 overexpression induced cell proliferation and invasion and inhibited cell apoptosis. Research conducted by Yu et al. [15] showed that LINC00673 was highly expressed in a significant proportion of human tongue squamous cell carcinoma samples and associated with poor prognosis.

Taken together, these findings shed light on an important functional interaction between LINC00673 and malignancies. Therefore, it would be interesting to examine the role of LINC00673 in neuroblastoma. With such purpose, we conducted the current study in the Chinese Han population. The current study has several important strengths. To the best of our knowledge, this is the first investigation to validate the association of neuroblastoma susceptibility with GWAS-identified polymorphism within LINC00673. The identification of LINC00673 as an antitumor factor in neuroblastoma was based on discoveries in GWASs in several tumors. Although our findings showed that the association between rs11655237 and neuroblastoma susceptibility were obtained in Chinese Han populations and are consistent with previous reports in other malignancies, further studies on this and other tumors in a different ethnic group would be beneficial. In addition, it has been suggested that rs11655237 might have a potential role in the regulation of gene expression via an enhancer, promoter, or silencer mechanism [9]. Therefore, further exploration of this issue should be addressed. Additionally, it would be intriguing to validate the effects of rs11655237 variation on the development of neuroblastoma using in vivo experimental settings.

Several limitations should be addressed in the present study. First, although it was the first study on the association between LINC00673 and neuroblastoma, we included only 393 neuroblastoma cases and 812 cancer-free controls. The relative small sample size may limit the statistical power. Replication studies from other centers with a larger sample size are encouraged to confirm the association. Second, only one polymorphism of the newly identified LINC00673 was investigated in the current study. More polymorphisms, especially the potentially functional polymorphisms not yet contained in previous GWASs, remain to be explored. Third, due to the design of the retrospective study, information bias and selection bias might be unavoidable. Because of the lack of information on dietary intake, living environmental factors, and parental exposures, only frequency matching of neuroblastoma cases and controls by age and gender could be used to reduce these biases. Fourth, in vitro and in vivo experiments should be performed to interrogate mechanism(s) underlying the association in the future. Finally, although recruited from two centers, including residents in Southern and Northern China, participants were all Han Chinese, so the results should be cautiously extrapolated to other ethnic groups.

In conclusion, our results verified that the LINC00673 rs11655237 C>T polymorphism was significantly associated with neuroblastoma susceptibility in the Chinese Han population, especially for children with neuroblastoma of the adrenal gland region and clinical stage IV. In the future, well-designed prospective studies with larger sample size including different ethnic populations, detailed information (including living environment, dietary intake, and parental exposures) and functional studies should be performed to strengthen our findings.

Funding

This work was supported by the Pearl River S&T Nova Program of Guangzhou [grant number 201710010086]; the Guangzhou Medical and Health Science and Technology Project [grant number 20161A010027]; the State Clinical Key Specialty Construction Project (Pediatric Surgery) 2013 [grant number GJLCZD1301]; the Guangzhou Science Technology and Innovation Commission [grant number 201607010395], and the Natural Science Foundation of Guangdong province [grant number 2016A030313496].

Competing interests

The authors declare that there are no competing interests associated with the manuscript.

Author contribution

All authors contributed significantly to this work. Z.Z., W.J., J.Z., R.Z. and T.Y. performed the research study and collected the data. J.H. and Y.C. analyzed the data. J.H., H.X. and Y.Z. designed the research study. Z.Z. and J.Z. wrote the paper. J.H. prepared all the tables. All authors reviewed the manuscript. In addition, all authors have read and approved the manuscript.

Abbreviations: CI, confidence interval; GWAS, genome-wide association study; INSS, International Neuroblastoma Staging System; lincRNA, long intergenic non-coding RNA; NSCLC, non-small-cell lung cancer; OR, odds ratio

  • © 2018 The Author(s).
http://creativecommons.org/licenses/by/4.0/

This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

References

  1. ↵
    1. Shohet J.,
    2. Foster J.
    (2017) Neuroblastoma. BMJ 357, j1863 doi:10.1136/bmj.j1863 pmid:28468760
    OpenUrlFREE Full Text
    1. Brodeur G.M.,
    2. Bagatell R.
    (2014) Mechanisms of neuroblastoma regression. Nat. Rev. Clin. Oncol. 11, 704–713 doi:10.1038/nrclinonc.2014.168 pmid:25331179
    OpenUrlCrossRefPubMed
  2. ↵
    1. Siegel R.L.,
    2. Miller K.D.,
    3. Jemal A.
    (2017) Cancer statistics, 2017. CA Cancer J. Clin. 67, 7–30 doi:10.3322/caac.21387 pmid:28055103
    OpenUrlCrossRefPubMed
  3. ↵
    1. Maris J.M.,
    2. Mosse Y.P.,
    3. Bradfield J.P.,
    4. Hou C.,
    5. Monni S.,
    (2008) Chromosome 6p22 locus associated with clinically aggressive neuroblastoma. N. Engl. J. Med. 358, 2585–2593 doi:10.1056/NEJMoa0708698 pmid:18463370
    OpenUrlCrossRefPubMedWeb of Science
  4. ↵
    1. Cordeau M.,
    2. Belounis A.,
    3. Lelaidier M.,
    4. Cordeiro P.,
    5. Sartelet H.,
    (2016) Efficient killing of high risk neuroblastoma using natural killer cells activated by plasmacytoid dendritic cells. PLoS ONE 11, e0164401 doi:10.1371/journal.pone.0164401 pmid:27716850
    OpenUrlCrossRefPubMed
  5. ↵
    1. Yu A.L.,
    2. Gilman A.L.,
    3. Ozkaynak M.F.,
    4. London W.B.,
    5. Kreissman S.G.,
    (2010) Anti-GD2 antibody with GM-CSF, interleukin-2, and isotretinoin for neuroblastoma. N. Engl. J. Med. 363, 1324–1334 doi:10.1056/NEJMoa0911123 pmid:20879881
    OpenUrlCrossRefPubMedWeb of Science
  6. ↵
    1. Yalcin B.,
    2. Kremer L.C.,
    3. van Dalen E.C.
    (2015) High-dose chemotherapy and autologous haematopoietic stem cell rescue for children with high-risk neuroblastoma. Cochrane Database Syst. Rev. CD006301, doi:10.1002/14651858.CD006301.pub3 pmid:26436598
    OpenUrlCrossRefPubMed
  7. ↵
    1. Peinemann F.,
    2. van Dalen E.C.,
    3. Tushabe D.A.,
    4. Berthold F.
    (2015) Retinoic acid post consolidation therapy for high-risk neuroblastoma patients treated with autologous hematopoietic stem cell transplantation. Cochrane Database Syst. Rev. 1, CD010685 pmid:25634649
    OpenUrlPubMed
  8. ↵
    1. Childs E.J.,
    2. Mocci E.,
    3. Campa D.,
    4. Bracci P.M.,
    5. Gallinger S.,
    (2015) Common variation at 2p13.3, 3q29, 7p13 and 17q25.1 associated with susceptibility to pancreatic cancer. Nat. Genet. 47, 911–916 doi:10.1038/ng.3341 pmid:26098869
    OpenUrlCrossRefPubMed
  9. ↵
    1. Zheng J.,
    2. Huang X.,
    3. Tan W.,
    4. Yu D.,
    5. Du Z.,
    (2016) Pancreatic cancer risk variant in LINC00673 creates a miR-1231 binding site and interferes with PTPN11 degradation. Nat. Genet. 48, 747–757 doi:10.1038/ng.3568 pmid:27213290
    OpenUrlCrossRefPubMed
  10. ↵
    1. Lu W.,
    2. Zhang H.,
    3. Niu Y.,
    4. Wu Y.,
    5. Sun W.,
    (2017) Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p. Mol. Cancer 16, 118 doi:10.1186/s12943-017-0685-9 pmid:28697764
    OpenUrlCrossRefPubMed
    1. Tan Q.,
    2. Yu Y.,
    3. Li N.,
    4. Jing W.,
    5. Zhou H.,
    (2017) Identification of long non-coding RNA 00312 and 00673 in human NSCLC tissues. Mol. Med. Rep. 16, 4721–4729 doi:10.3892/mmr.2017.7196 pmid:28849087
    OpenUrlCrossRefPubMed
  11. ↵
    1. Lu W.,
    2. Zhang H.,
    3. Niu Y.,
    4. Wu Y.,
    5. Sun W.,
    (2017) Erratum to: Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p. Mol. Cancer 16, 144 doi:10.1186/s12943-017-0716-6 pmid:28851432
    OpenUrlCrossRefPubMed
  12. ↵
    1. Huang M.,
    2. Hou J.,
    3. Wang Y.,
    4. Xie M.,
    5. Wei C.,
    (2017) Long noncoding RNA LINC00673 is activated by SP1 and exerts oncogenic properties by interacting with LSD1 and EZH2 in gastric cancer. Mol. Ther. 25, 1014–1026 doi:10.1016/j.ymthe.2017.01.017 pmid:28214253
    OpenUrlCrossRefPubMed
  13. ↵
    1. Yu J.,
    2. Liu Y.,
    3. Gong Z.,
    4. Zhang S.,
    5. Guo C.,
    (2017) Overexpression long non-coding RNA LINC00673 is associated with poor prognosis and promotes invasion and metastasis in tongue squamous cell carcinoma. Oncotarget 8, 16621–16632 pmid:28039470
    OpenUrlPubMed
  14. ↵
    1. Abdul-Rahman U.,
    2. Gyorffy B.,
    3. Adams B.D.
    (2017) linc00673 (ERRLR01) is a prognostic indicator of overall survival in breast cancer. Transcription, doi:10.1080/21541264.2017.1329684
    OpenUrlCrossRef
  15. ↵
    1. Zhang J.,
    2. Lin H.,
    3. Wang J.,
    4. He J.,
    5. Zhang D.,
    (2017) LMO1 polymorphisms reduce neuroblastoma risk in Chinese children: a two-center case-control study. Oncotarget 8, 65620–65626 pmid:29029458
    OpenUrlPubMed
    1. He J.,
    2. Wang F.,
    3. Zhu J.,
    4. Zhang Z.,
    5. Zou Y.,
    (2017) The TP53 gene rs1042522 C>G polymorphism and neuroblastoma risk in Chinese children. Aging (Albany N.Y.) 9, 852–859 pmid:28275206
    OpenUrlPubMed
    1. He J.,
    2. Zou Y.,
    3. Wang T.,
    4. Zhang R.,
    5. Yang T.,
    (2017) Genetic variations of GWAS-identified genes and neuroblastoma susceptibility: a replication study in Southern Chinese children. Transl. Oncol. 10, 936–941 doi:10.1016/j.tranon.2017.09.008 pmid:29024823
    OpenUrlCrossRefPubMed
  16. ↵
    1. He J.,
    2. Wang F.,
    3. Zhu J.,
    4. Zhang R.,
    5. Yang T.,
    (2016) Association of potentially functional variants in the XPG gene with neuroblastoma risk in a Chinese population. J. Cell. Mol. Med. 20, 1481–1490 doi:10.1111/jcmm.12836 pmid:27019310
    OpenUrlCrossRefPubMed
  17. ↵
    1. He J.,
    2. Zhang R.,
    3. Zou Y.,
    4. Zhu J.,
    5. Yang T.,
    (2016) Evaluation of GWAS-identified SNPs at 6p22 with neuroblastoma susceptibility in a Chinese population. Tumour Biol. 37, 1635–1639 doi:10.1007/s13277-015-3936-7 pmid:26307394
    OpenUrlCrossRefPubMed
  18. ↵
    1. Li J.,
    2. Zou L.,
    3. Zhou Y.,
    4. Li L.,
    5. Zhu Y.,
    (2017) A low-frequency variant in SMAD7 modulates TGF-beta signaling and confers risk for colorectal cancer in Chinese population. Mol. Carcinog. 56, 1798–1807 doi:10.1002/mc.22637 pmid:28218435
    OpenUrlCrossRefPubMed
    1. Lou J.,
    2. Gong J.,
    3. Ke J.,
    4. Tian J.,
    5. Zhang Y.,
    (2017) A functional polymorphism located at transcription factor binding sites, rs6695837 near LAMC1 gene, confers risk of colorectal cancer in Chinese populations. Carcinogenesis 38, 177–183 pmid:28039327
    OpenUrlPubMed
  19. ↵
    1. He J.,
    2. Qiu L.X.,
    3. Wang M.Y.,
    4. Hua R.X.,
    5. Zhang R.X.,
    (2012) Polymorphisms in the XPG gene and risk of gastric cancer in Chinese populations. Hum. Genet. 131, 1235–1244 doi:10.1007/s00439-012-1152-8 pmid:22371296
    OpenUrlCrossRefPubMed
  20. ↵
    1. Brodeur G.M.,
    2. Pritchard J.,
    3. Berthold F.,
    4. Carlsen N.L.,
    5. Castel V.,
    (1994) Revisions of the international criteria for neuroblastoma diagnosis, staging and response to treatment. Prog. Clin. Biol. Res. 385, 363–369 pmid:7972232
    OpenUrlPubMed
  21. ↵
    1. Tsai M.C.,
    2. Spitale R.C.,
    3. Chang H.Y.
    (2011) Long intergenic noncoding RNAs: new links in cancer progression. Cancer Res. 71, 3–7 doi:10.1158/0008-5472.CAN-10-2483 pmid:21199792
    OpenUrlAbstract/FREE Full Text
  22. ↵
    1. Gibb E.A.,
    2. Brown C.J.,
    3. Lam W.L.
    (2011) The functional role of long non-coding RNA in human carcinomas. Mol. Cancer 10, 38 doi:10.1186/1476-4598-10-38 pmid:21489289
    OpenUrlCrossRefPubMed
  23. ↵
    1. Cabili M.N.,
    2. Trapnell C.,
    3. Goff L.,
    4. Koziol M.,
    5. Tazon-Vega B.,
    (2011) Integrative annotation of human large intergenic noncoding RNAs reveals global properties and specific subclasses. Genes Dev. 25, 1915–1927 doi:10.1101/gad.17446611 pmid:21890647
    OpenUrlAbstract/FREE Full Text
  24. ↵
    1. Leighton P.A.,
    2. Ingram R.S.,
    3. Eggenschwiler J.,
    4. Efstratiadis A.,
    5. Tilghman S.M.
    (1995) Disruption of imprinting caused by deletion of the H19 gene region in mice. Nature 375, 34–39 doi:10.1038/375034a0 pmid:7536897
    OpenUrlCrossRefPubMedWeb of Science
  25. ↵
    1. Pandey R.R.,
    2. Mondal T.,
    3. Mohammad F.,
    4. Enroth S.,
    5. Redrup L.,
    (2008) Kcnq1ot1 antisense noncoding RNA mediates lineage-specific transcriptional silencing through chromatin-level regulation. Mol. Cell 32, 232–246 doi:10.1016/j.molcel.2008.08.022 pmid:18951091
    OpenUrlCrossRefPubMedWeb of Science
  26. ↵
    1. Ji P.,
    2. Diederichs S.,
    3. Wang W.,
    4. Boing S.,
    5. Metzger R.,
    (2003) MALAT-1, a novel noncoding RNA, and thymosin beta4 predict metastasis and survival in early-stage non-small cell lung cancer. Oncogene 22, 8031–8041 doi:10.1038/sj.onc.1206928 pmid:12970751
    OpenUrlCrossRefPubMedWeb of Science
  27. ↵
    1. Rinn J.L.,
    2. Kertesz M.,
    3. Wang J.K.,
    4. Squazzo S.L.,
    5. Xu X.,
    (2007) Functional demarcation of active and silent chromatin domains in human HOX loci by noncoding RNAs. Cell 129, 1311–1323 doi:10.1016/j.cell.2007.05.022 pmid:17604720
    OpenUrlCrossRefPubMedWeb of Science
  28. ↵
    1. Heo J.B.,
    2. Sung S.
    (2011) Vernalization-mediated epigenetic silencing by a long intronic noncoding RNA. Science 331, 76–79 doi:10.1126/science.1197349 pmid:21127216
    OpenUrlAbstract/FREE Full Text
  29. ↵
    1. Zhao J.,
    2. Sun B.K.,
    3. Erwin J.A.,
    4. Song J.J.,
    5. Lee J.T.
    (2008) Polycomb proteins targeted by a short repeat RNA to the mouse X chromosome. Science 322, 750–756 doi:10.1126/science.1163045 pmid:18974356
    OpenUrlAbstract/FREE Full Text
  30. ↵
    1. Yu W.,
    2. Gius D.,
    3. Onyango P.,
    4. Muldoon-Jacobs K.,
    5. Karp J.,
    (2008) Epigenetic silencing of tumour suppressor gene p15 by its antisense RNA. Nature 451, 202–206 doi:10.1038/nature06468 pmid:18185590
    OpenUrlCrossRefPubMedWeb of Science
  31. ↵
    1. Poliseno L.,
    2. Salmena L.,
    3. Zhang J.,
    4. Carver B.,
    5. Haveman W.J.,
    (2010) A coding-independent function of gene and pseudogene mRNAs regulates tumour biology. Nature 465, 1033–1038 doi:10.1038/nature09144 pmid:20577206
    OpenUrlCrossRefPubMedWeb of Science
  32. ↵
    1. Tseng R.C.,
    2. Chang J.W.,
    3. Hsien F.J.,
    4. Chang Y.H.,
    5. Hsiao C.F.,
    (2005) Genomewide loss of heterozygosity and its clinical associations in non small cell lung cancer. Int. J. Cancer 117, 241–247 doi:10.1002/ijc.21178 pmid:15900585
    OpenUrlCrossRefPubMedWeb of Science
  33. ↵
    (2016) A LincRNA risk variant promotes pancreatic tumorigenesis. Cancer Discov. 6, OF14 doi:10.1158/2159-8290.CD-RW2016-101 pmid:27080335
    OpenUrlAbstract/FREE Full Text
  34. ↵
    1. Shi X.,
    2. Ma C.,
    3. Zhu Q.,
    4. Yuan D.,
    5. Sun M.,
    (2016) Upregulation of long intergenic noncoding RNA 00673 promotes tumor proliferation via LSD1 interaction and repression of NCALD in non-small-cell lung cancer. Oncotarget 7, 25558–25575 pmid:27027352
    OpenUrlPubMed
  35. ↵
    1. Ma C.,
    2. Wu G.,
    3. Zhu Q.,
    4. Liu H.,
    5. Yao Y.,
    (2017) Long intergenic noncoding RNA 00673 promotes non-small-cell lung cancer metastasis by binding with EZH2 and causing epigenetic silencing of HOXA5. Oncotarget 8, 32696–32705 pmid:28423732
    OpenUrlPubMed
View Abstract
Previous ArticleNext Article
Back to top

February 2018

Volume: 38 Issue: 1

Bioscience Reports: 38 (1)
  • Table of Contents
  • About the Cover
  • Index by author

Actions

Email

Thank you for your interest in spreading the word about Bioscience Reports.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
LINC00673 rs11655237 C>T confers neuroblastoma susceptibility in Chinese population
(Your Name) has forwarded a page to you from Bioscience Reports
(Your Name) thought you would like to see this page from the Bioscience Reports web site.
Share
LINC00673 rs11655237 C>T confers neuroblastoma susceptibility in Chinese population
Zhuorong Zhang, Yitian Chang, Wei Jia, Jiao Zhang, Ruizhong Zhang, Jinhong Zhu, Tianyou Yang, Huimin Xia, Yan Zou, Jing He
Bioscience Reports Feb 2018, 38 (1) BSR20171667; DOI: 10.1042/BSR20171667
del.icio.us logo Digg logo Reddit logo Technorati logo Twitter logo CiteULike logo Facebook logo Mendeley logo
Citation Tools
LINC00673 rs11655237 C>T confers neuroblastoma susceptibility in Chinese population
Zhuorong Zhang, Yitian Chang, Wei Jia, Jiao Zhang, Ruizhong Zhang, Jinhong Zhu, Tianyou Yang, Huimin Xia, Yan Zou, Jing He
Bioscience Reports Feb 2018, 38 (1) BSR20171667; DOI: 10.1042/BSR20171667

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Print
Alerts

Please log in to add an alert for this article.

Request Permissions
Save to my folders

View Full PDF

 Open in Utopia Docs
  • Tweet Widget
  • Facebook Like

Jump To

  • Article
    • Abstract
    • Introduction
    • Methods
    • Results
    • Discussion
    • Funding
    • Competing interests
    • Author contribution
    • References
  • Figures
  • Info & Metrics
  • Supplementary Data
  • PDF

Keywords

LINC00673
neuroblastoma
polymorphism
Susceptibility

Related Articles

Cited By...

  • Portland Press Homepage
  • Publish With Us
  • Advertising
  • Technical Support
  • Bioscience Reports
  • Biochemical Journal
  • Clinical Science
  • Neuronal Signaling
  • Essays in Biochemistry
  • Emerging Topics in Life Sciences
  • Biochemical Society Transactions
  • Biochemical Society Symposia
  • Cell Signalling Biology

Portland Press Limited
Charles Darwin House
12 Roger Street
London WC1N 2JU
Email: editorial@portlandpress.com

The Biochemical Society