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Association Between miR-492 rs2289030 G>C and Susceptibility to Neuroblastoma in Chinese Children from Jiangsu Province

  • Wei-Jing Wang1,2,#,
  • Chun-Lei Zhou3,#,
  • Xin-Xin Zhang1,
  • Ye-Mu Zhao4,
  • Chang-Mi Deng1,
  • Hai-Yan Wu3,
  • Zhen-Jian Zhuo1,5,*  and
  • Jing He1,* 
 Author information  Cite
Cancer Screening and Prevention   2023;2(4):199-203

doi: 10.14218/CSP.2023.00025S

Abstract

Background and objectives

Neuroblastoma is a heterogeneous solid tumor that originates extracranially from neuroblasts. Previous research has demonstrated that miR-492 polymorphisms can contribute to cancer susceptibility. However, their specific involvement in susceptibility to neuroblastoma has yet to be fully clarified.

Methods

To address this question, we used the TaqMan method to genotype miR-492 rs2289030 G>C in a cohort of 402 neuroblastoma children and 473 control individuals from Jiangsu Province, China.

Results

Our study showed that there was no significant association between miR-492 rs2289030 G>C and the risk of neuroblastoma in children, as assessed by combined odds ratios (ORs) and 95% confidence intervals (P > 0.05).

Conclusions

Further validation of these findings requires well-designed studies with large sample sizes.

Keywords

miR-492, Susceptibility, Neuroblastoma, Polymorphism

Introduction

Neuroblastoma is a heterogeneous solid tumor that originates extracranially from neuroblasts. Approximately 90% of affected individuals are under the age of 10, with a median diagnosis age of 18 months, ultimately leading to the development of tumors in the adrenal glands and/or sympathetic ganglia.1 The overall survival rate for children aged between 18 months and 12 years is 49%, whereas it decreases to less than 10% for adolescents and young adults (>12 years).2 The prognosis of patients with neuroblastoma varies significantly. While some patients may recover spontaneously without any medical intervention (as observed in 4S neuroblastoma), others need to fight drug resistance throughout their lives.3,4 Following disease staging, each patient is categorized into one of the four groups: very-low-risk, low-risk, intermediate-risk, or high-risk based on clinical and molecular risk factors. This approach helps clinicians determine the optimal treatment approach.5 Despite advancements in overall survival rates, 36% of patients are diagnosed with metastatic, high-risk disease, which poses significant challenges for successful treatment.6 The prognosis for high-risk neuroblastoma patients remains dismal, with an overall 5-year survival rate of less than 50%, even after aggressive surgery and multimodal cytotoxic therapies.7

The specific environmental risk factors associated with the development of neuroblastoma are still undefined.8 Multiple studies have suggested that genetic factors, including ALK9,10 and PHOX2B11,12 gene mutations, may have a significant impact on the development of neuroblastoma. Genome-wide association studies (GWASs) have additionally discovered polymorphisms within the CASC15, HACE1, LMO1, LIN28B, BARD1, and TP53 genes that are associated with an increased risk of neuroblastoma.5,13,14 The identification of microRNAs (miRNAs) has revealed a novel mechanism of gene regulation, shedding light on the complex pathophysiology of neuroblastoma and potentially offering solutions to unresolved issues. miRNAs are short, single-stranded RNA molecules consisting of 19–25 nucleotides in length.15 miRNAs act by binding to a complementary sequence located in the 3′ untranslated region of mRNAs, thereby inhibiting gene expression, causing mRNA degradation, and preventing translation.16 Dysregulation of miRNAs has been observed in various types of malignancies, where specific miRNAs can function either as tumor promoters or tumor suppressors.17,18 Single nucleotide polymorphisms (SNPs) within the encoding sequences of precursor miRNAs (pre-miRNAs) can potentially impact the expression and maturation of miRNAs, consequently affecting susceptibility to neuroblastoma and other types of cancers.19–22

In this study, we focused on miRNA-492, which has been reported to be a regulator involved in several gastrointestinal cancers.23 Previous studies have also suggested that the miRNA-492 G>C rs2289030 polymorphism could impact susceptibility to different types of liver cancers, such as hepatocellular carcinoma.24

However, to date, no study has investigated the role of miRNA-492 G>C rs2289030 in the risk of neuroblastoma. We conducted this case-control investigation using samples from Nanjing Children’s Hospital, comprising 402 cases and 473 controls. The aim was to evaluate the potential link between miRNA-492 G>C rs2289030 and neuroblastoma susceptibility.

Methods

Study subjects

This study involved a sample of 402 cases of neuroblastoma and 473 healthy control subjects enrolled from Jiangsu province (Table S1). This study was conducted in accordance with the ethical principles outlined in the Declaration of Helsinki (revised in 2013). The study protocol (202112141-1) was approved by the institutional review board of the Children’s Hospital of Nanjing Medical University. Prior to participation, all individuals involved in the study, including minors, provided written informed consent. For participants who were minors, the consent form was signed by their parent or legal guardian. Details of the participant selection process have been provided in our previous publication.14,25,26

Genotyping of the miR-492 rs2289030 G>C SNP

Based on our previously established criteria,27 we chose to investigate the potential association of the miR-492 rs2289030 G>C polymorphism in this case-control study. We extracted genomic DNA from peripheral blood donated by subjects using the TIANamp Blood DNA Kit (TianGen Biotech Co. Ltd., Beijing, China). The genotyping of all selected SNP was performed using a commercially available TaqMan real-time PCR assay (ID C_15880380_10) according to standard protocols. We programmed the instrument for PCR using the following conditions: pre-read stage at 60°C for 30 seconds, holding stage at 95°C for 10 minutes, and 45 cycles of denaturation at 95°C for 15 seconds, annealing and extension at 60°C for 1 minute. Then, we selected standard run mode and added the reaction mixture (5 µL for each well in a 384-well reaction plate). The reaction plate was loaded into the instrument, and the run was started. Additional methodological details can be found in the referenced literature.27–29 Eight negative controls with water and eight replicate samples were included in each 384-well plate as a quality control measure. In addition, 10% of the samples were randomly selected for a second run. All duplicate sets were found to have a concordance rate of 100%.

Statistical analysis

The demographic characteristics and distribution of genotype frequencies between patients with neuroblastoma and controls were compared using the bilateral χ2 test. The goodness-of-fit χ2 test was used to assess whether there were deviations from Hardy-Weinberg equilibrium for the selected polymorphisms in the control group. Then, we used a two-sided chi-square test to assess the differences in demographic variables and allele frequencies between all cases and controls. Logistic regression analysis was used to evaluate the relationship between the miR-492 SNP and neuroblastoma susceptibility, and odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. All statistical analyses were carried out using SAS software version 9.4 (SAS Institute, Cary, NC). The level of statistical significance was predetermined at P < 0.05.

Results

Characteristics of the participants

This study included a total of 402 neuroblastoma cases and 473 healthy controls from Jiangsu province. All of the cases included in this study were newly confirmed neuroblastoma patients who underwent histopathological diagnosis and had no progressive disease or previous treatments. The location of the patients’ neuroblastoma was mainly in the retroperitoneal region (41.54%), mediastinum (29.85%) and adrenal gland (23.13%). International Neuroblastoma Staging System (INSS) staging consisted primarily of stage I (26.87%) and stage IV (25.87%). The clinical characteristics and demographics of neuroblastoma cases and controls are summarized in Table S1. No significant associations were detected between cases and controls in terms of age (P = 0.100) and gender (P = 0.987).

Association of the miR-492 SNP with susceptibility to neuroblastoma

As shown in Table 1, the genotype frequency distribution of miR-492 rs2289030 G>C was in accordance with the Hardy-Weinberg equilibrium (HWE) in the control group (P = 0.056). Our findings revealed that the genotype distribution among neuroblastoma patients did not show significant differences when compared with those among the control group. Consequently, none of the rs2289030 genotypes were found to be associated with susceptibility to neuroblastoma.

Table 1

miR-492 rs2289030 G>C polymorphism and neuroblastoma risk in children from Jiangsu province

GenotypeCases (N = 402)Controls (N = 473)PaCrude OR (95% CI)PAdjusted OR (95% CI)bPb
rs2289030 (HWE = 0.056)
  GG248 (61.69)286 (60.47)1.001.00
  GC134 (33.33)154 (32.56)1.00 (0.75–1.34)0.9811.00 (0.75–1.34)0.982
  CC20 (4.98)33 (6.98)0.70 (0.39–1.25)0.2270.70 (0.39–1.25)0.227
  Additive0.4340.92 (0.74–1.14)0.4330.92 (0.74–1.14)0.433
  Dominant154 (38.31)187 (39.53)0.7110.95 (0.72–1.25)0.7110.95 (0.72–1.25)0.711
  GG/GC382 (95.02)440 (93.03)1.001.00
  CC20 (4.98)33 (6.98)0.2160.70 (0.39–1.24)0.2180.70 (0.39–1.24)0.218

Discussion

In this case-control study involving children from Jiangsu province, China, we examined the association between a miR-492 SNP and susceptibility to neuroblastoma. To the best of our knowledge, miR-492 rs2289030 G>C has not been investigated in any previous studies regarding neuroblastoma. As a result, our study found no significant association between miR-492 rs2289030 G>C and the risk of neuroblastoma in children.

With the progress in research and technology, an increasing number of researchers support the significant involvement of genetic factors in the pathogenesis of neuroblastoma. In recent years, GWASs have identified a number of genetic variants located in various genes that are linked to neuroblastoma risk.30–34 The majority of the SNPs identified by GWAS as contributing to neuroblastoma risk have been verified through replication case-control studies.25,26,35–37 It is necessary to further identify gene polymorphisms that are associated with susceptibility to neuroblastoma, which will aid in comprehending the etiology of this disease.

miRNAs can negatively regulate gene expression at the posttranscriptional level, thereby impacting various cellular processes, such as cell proliferation, carcinogenesis, apoptosis, metabolism, and differentiation.38 miR-492 is derived from both the KRT19 pseudogene 2 and the KRT19 transcript.39,40 It exerts its influence by targeting 11 genes and playing a role in multiple signaling pathways, governing crucial cellular processes such as invasion, epithelial-mesenchymal transition, cell proliferation, migration, and apoptosis.41 However, miR-492 exhibits increased expression in multiple cancer types, while in certain others, its expression is decreased.42–45 Neither the GG, GC, nor CC risk genotypes in our study showed any correlation with neuroblastoma risk. The reasons for the differential expression of miR-492 in various cancers are not fully understood, and further studies with larger sample sizes are needed. Consistent with our results, studies exploring miR-492 rs2289030 G>C genotype and susceptibility to colorectal cancer46 and gastric cancer47 failed to find an association, as did Hirschsprung disease48 and high-risk atrophic gastritis.47 The participants in these studies were European or southern Chinese. Polymorphisms may have varying genetic effects on cancer susceptibility contingent on factors such as the type of cancer, ethnicity, and geographical location.

This study has several limitations that should be acknowledged. Firstly, the statistical power of this study might be compromised due to the relatively small sample size. Secondly, as a hospital-based case-control study, the inclusion of non-representative subjects could lead to inherent selection bias. Thirdly, the conclusions drawn from this study may lack generalizability, as the subjects solely consisted of individuals of Chinese descent. Fourthly, the selection of the SNP was based on prior knowledge of potentially functional SNPs, probably resulting in the omission of other crucial tagging SNPs. Finally, in the current study, assessments of environmental factors and gene-environment interactions were not possible due to the lack of available environmental data.

Conclusions

We present initial evidence indicating that polymorphisms in the miR-492 rs2289030 G>C genotype may not have an impact on the risk of neuroblastoma in individuals from Jiangsu province, China. Additional validation of this evidence with larger samples is required. Ultimately, our study may shed light on the role of miR-492 in this aggressive pediatric tumor.

Supporting information

Supplementary material for this article is available at https://doi.org/10.14218/CSP.2023.00025S .

Table S1

Demographic characteristics of neuroblastoma patients and cancer-free controls from Jiangsu province.

(DOCX)

Abbreviations

CIs: 

confidence intervals

GWASs: 

genome-wide association studies

HWE: 

Hardy-Weinberg equilibrium

miRNAs: 

microRNAs

ORs: 

odds ratios

pre-miRNAs: 

precursor miRNAs

SNPs: 

single nucleotide polymorphisms

INSS: 

International Neuroblastoma Staging System

Declarations

Acknowledgement

None.

Ethical statement

This study was conducted in accordance with the ethical principles outlined in the Declaration of Helsinki (revised in 2013). The study protocol (202112141-1) was approved by the institutional review board of the Children’s Hospital of Nanjing Medical University. Prior to participation, all individuals involved in the study, including minors, provided written informed consent. For participants who were minors, the consent form was signed by their parent or legal guardian.

Data sharing statement

The corresponding author will provide access to the datasets generated and utilized during the study upon reasonable request.

Funding

This study was supported by grants from the National Natural Science Foundation of China (No: 82173593, 82002636), the Postdoctoral Science Foundation of Jiangsu Province (No: 2021K524C), and the Science, Technology and Innovation Commission of Shenzhen (No: JCYJ20220531093213030).

Conflict of interest

One of the authors, Prof. Jing He, has been an editorial board member of Cancer Screening and Prevention since April 2023. The authors have no conflict of interests related to this publication.

Authors’ contributions

Contributed to study concept and design (ZJZ and JH), acquisition of the data (WJW and CLZ), assay performance and data analysis (WJW, CLZ, XXZ, YMZ, CMD, and HYW), drafting of the manuscript (WJW and CLZ), critical revision of the manuscript (ZJZ and JH), and supervision (ZJZ and JH).

References

  1. London WB, Castleberry RP, Matthay KK, Look AT, Seeger RC, Shimada H, et al. Evidence for an age cutoff greater than 365 days for neuroblastoma risk group stratification in the Children’s Oncology Group. J Clin Oncol 2005;23(27):6459-6465 View Article PubMed/NCBI
  2. Zeineldin M, Patel AG, Dyer MA. Neuroblastoma: When differentiation goes awry. Neuron 2022;110(18):2916-2928 View Article PubMed/NCBI
  3. Maris JM. Recent advances in neuroblastoma. N Engl J Med 2010;362(23):2202-2211 View Article PubMed/NCBI
  4. Kawano A, Hazard FK, Chiu B, Naranjo A, LaBarre B, London WB, et al. Stage 4S Neuroblastoma: Molecular, Histologic, and Immunohistochemical Characteristics and Presence of 2 Distinct Patterns of MYCN Protein Overexpression-A Report From the Children’s Oncology Group. Am J Surg Pathol 2021;45(8):1075-1081 View Article PubMed/NCBI
  5. Matthay KK, Maris JM, Schleiermacher G, Nakagawara A, Mackall CL, Diller L, et al. Neuroblastoma. Nat Rev Dis Primers 2016;2:16078 View Article PubMed/NCBI
  6. Cohn SL, Pearson AD, London WB, Monclair T, Ambros PF, Brodeur GM, et al. The International Neuroblastoma Risk Group (INRG) classification system: an INRG Task Force report. J Clin Oncol 2009;27(2):289-297 View Article PubMed/NCBI
  7. Irwin MS, Park JR. Neuroblastoma: paradigm for precision medicine. Pediatr Clin North Am 2015;62(1):225-256 View Article PubMed/NCBI
  8. Patton T, Olshan AF, Neglia JP, Castleberry RP, Smith J. Parental exposure to medical radiation and neuroblastoma in offspring. Paediatr Perinat Epidemiol 2004;18(3):178-185 View Article PubMed/NCBI
  9. Chen Y, Takita J, Choi YL, Kato M, Ohira M, Sanada M, et al. Oncogenic mutations of ALK kinase in neuroblastoma. Nature 2008;455(7215):971-974 View Article PubMed/NCBI
  10. George RE, Sanda T, Hanna M, Fröhling S, Luther W, Zhang J, et al. Activating mutations in ALK provide a therapeutic target in neuroblastoma. Nature 2008;455(7215):975-978 View Article PubMed/NCBI
  11. Mosse YP, Laudenslager M, Khazi D, Carlisle AJ, Winter CL, Rappaport E, et al. Germline PHOX2B mutation in hereditary neuroblastoma. Am J Hum Genet 2004;75(4):727-730 View Article PubMed/NCBI
  12. Bourdeaut F, Trochet D, Janoueix-Lerosey I, Ribeiro A, Deville A, Coz C, et al. Germline mutations of the paired-like homeobox 2B (PHOX2B) gene in neuroblastoma. Cancer Lett 2005;228(1-2):51-58 View Article PubMed/NCBI
  13. Tolbert VP, Coggins GE, Maris JM. Genetic susceptibility to neuroblastoma. Curr Opin Genet Dev 2017;42:81-90 View Article PubMed/NCBI
  14. He J, Zou Y, Wang T, Zhang R, Yang T, Zhu J, et al. Genetic Variations of GWAS-Identified Genes and Neuroblastoma Susceptibility: a Replication Study in Southern Chinese Children. Transl Oncol 2017;10(6):936-941 View Article PubMed/NCBI
  15. Vishnoi A, Rani S. MiRNA Biogenesis and Regulation of Diseases: An Overview. Methods Mol Biol 2017;1509:1-10 View Article PubMed/NCBI
  16. Bartel DP. MicroRNAs: target recognition and regulatory functions. Cell 2009;136(2):215-233 View Article PubMed/NCBI
  17. Anvarnia A, Mohaddes-Gharamaleki F, Asadi M, Akbari M, Yousefi B, Shanehbandi D. Dysregulated microRNAs in colorectal carcinogenesis: New insight to cell survival and apoptosis regulation. J Cell Physiol 2019;234(12):21683-21693 View Article PubMed/NCBI
  18. Xu J, Meng Q, Li X, Yang H, Xu J, Gao N, et al. Long Noncoding RNA MIR17HG Promotes Colorectal Cancer Progression via miR-17-5p. Cancer Res 2019;79(19):4882-4895 View Article PubMed/NCBI
  19. Sung JH, Kim SH, Yang WI, Kim WJ, Moon JY, Kim IJ, et al. miRNA polymorphisms (miR-146a, miR-149, miR-196a2 and miR-499) are associated with the risk of coronary artery disease. Mol Med Rep 2016;14(3):2328-2342 View Article PubMed/NCBI
  20. Yin J, Wang X, Zheng L, Shi Y, Wang L, Shao A, et al. Hsa-miR-34b/c rs4938723 T>C and hsa-miR-423 rs6505162 C>A polymorphisms are associated with the risk of esophageal cancer in a Chinese population. PLoS One 2013;8(11):e80570 View Article PubMed/NCBI
  21. Mishra PJ, Humeniuk R, Mishra PJ, Longo-Sorbello GS, Banerjee D, Bertino JR. A miR-24 microRNA binding-site polymorphism in dihydrofolate reductase gene leads to methotrexate resistance. Proc Natl Acad Sci U S A 2007;104(33):13513-13518 View Article PubMed/NCBI
  22. He J, Zou Y, Liu X, Zhu J, Zhang J, Zhang R, et al. Association of Common Genetic Variants in Pre-microRNAs and Neuroblastoma Susceptibility: A Two-Center Study in Chinese Children. Mol Ther Nucleic Acids 2018;11:1-8 View Article PubMed/NCBI
  23. Naccarati A, Pardini B, Stefano L, Landi D, Slyskova J, Novotny J, et al. Polymorphisms in miRNA-binding sites of nucleotide excision repair genes and colorectal cancer risk. Carcinogenesis 2012;33(7):1346-1351 View Article PubMed/NCBI
  24. Al-Qahtani AA, Al-Anazi MR, Nazir N, Wani K, Abdo AA, Sanai FM, et al. Association of single nucleotide polymorphisms in microRNAs with susceptibility to hepatitis B virus infection and HBV-related liver complications: A study in a Saudi Arabian population. J Viral Hepat 2017;24(12):1132-1142 View Article PubMed/NCBI
  25. He J, Wang F, Zhu J, Zhang Z, Zou Y, Zhang R, et al. The TP53 gene rs1042522 C>G polymorphism and neuroblastoma risk in Chinese children. Aging (Albany NY) 2017;9(3):852-859 View Article PubMed/NCBI
  26. He J, Yang T, Zhang R, Zhu J, Wang F, Zou Y, et al. Potentially functional polymorphisms in the LIN28B gene contribute to neuroblastoma susceptibility in Chinese children. J Cell Mol Med 2016;20(8):1534-1541 View Article PubMed/NCBI
  27. He J, Qiu LX, Wang MY, Hua RX, Zhang RX, Yu HP, et al. Polymorphisms in the XPG gene and risk of gastric cancer in Chinese populations. Hum Genet 2012;131(7):1235-1244 View Article PubMed/NCBI
  28. Gong J, Tian J, Lou J, Wang X, Ke J, Li J, et al. A polymorphic MYC response element in KBTBD11 influences colorectal cancer risk, especially in interaction with an MYC-regulated SNP rs6983267. Ann Oncol 2018;29(3):632-639 View Article PubMed/NCBI
  29. Li J, Zou L, Zhou Y, Li L, Zhu Y, Yang Y, et al. A low-frequency variant in SMAD7 modulates TGF-β signaling and confers risk for colorectal cancer in Chinese population. Mol Carcinog 2017;56(7):1798-1807 View Article PubMed/NCBI
  30. Diskin SJ, Capasso M, Schnepp RW, Cole KA, Attiyeh EF, Hou C, et al. Common variation at 6q16 within HACE1 and LIN28B influences susceptibility to neuroblastoma. Nat Genet 2012;44(10):1126-1130 View Article PubMed/NCBI
  31. Diskin SJ, Capasso M, Diamond M, Oldridge DA, Conkrite K, Bosse KR, et al. Rare variants in TP53 and susceptibility to neuroblastoma. J Natl Cancer Inst 2014;106(4):dju047 View Article PubMed/NCBI
  32. Wang K, Diskin SJ, Zhang H, Attiyeh EF, Winter C, Hou C, et al. Integrative genomics identifies LMO1 as a neuroblastoma oncogene. Nature 2011;469(7329):216-220 View Article PubMed/NCBI
  33. Nguyen le B, Diskin SJ, Capasso M, Wang K, Diamond MA, Glessner J, et al. Phenotype restricted genome-wide association study using a gene-centric approach identifies three low-risk neuroblastoma susceptibility Loci. PLoS Genet 2011;7(3):e1002026 View Article PubMed/NCBI
  34. Zhuo ZJ, Liu W, Zhang J, Zhu J, Zhang R, Tang J, et al. Functional Polymorphisms at ERCC1/XPF Genes Confer Neuroblastoma Risk in Chinese Children. EBioMedicine 2018;30:113-119 View Article PubMed/NCBI
  35. He J, Zhong W, Zeng J, Zhu J, Zhang R, Wang F, et al. LMO1 gene polymorphisms contribute to decreased neuroblastoma susceptibility in a Southern Chinese population. Oncotarget 2016;7(16):22770-22778 View Article PubMed/NCBI
  36. Zhang R, Zou Y, Zhu J, Zeng X, Yang T, Wang F, et al. The Association between GWAS-identified BARD1 Gene SNPs and Neuroblastoma Susceptibility in a Southern Chinese Population. Int J Med Sci 2016;13(2):133-138 View Article PubMed/NCBI
  37. Zhang J, Lin H, Wang J, He J, Zhang D, Qin P, et al. LMO1 polymorphisms reduce neuroblastoma risk in Chinese children: a two-center case-control study. Oncotarget 2017;8(39):65620-65626 View Article PubMed/NCBI
  38. Calin GA, Croce CM. MicroRNA signatures in human cancers. Nat Rev Cancer 2006;6(11):857-866 View Article PubMed/NCBI
  39. Bentwich I, Avniel A, Karov Y, Aharonov R, Gilad S, Barad O, et al. Identification of hundreds of conserved and nonconserved human microRNAs. Nat Genet 2005;37(7):766-770 View Article PubMed/NCBI
  40. von Frowein J, Pagel P, Kappler R, von Schweinitz D, Roscher A, Schmid I. MicroRNA-492 is processed from the keratin 19 gene and up-regulated in metastatic hepatoblastoma. Hepatology 2011;53(3):833-842 View Article PubMed/NCBI
  41. Shen J, Si J, Wang Q, Mao Y, Gao W, Duan S. Current status and future perspectives in dysregulated miR-492. Gene 2023;877:147518 View Article PubMed/NCBI
  42. Wu A, Wu K, Li M, Bao L, Shen X, Li S, et al. Upregulation of microRNA-492 induced by epigenetic drug treatment inhibits the malignant phenotype of clear cell renal cell carcinoma in vitro. Mol Med Rep 2015;12(1):1413-1420 View Article PubMed/NCBI
  43. Schulten HJ, Alotibi R, Al-Ahmadi A, Ata M, Karim S, Huwait E, et al. Effect of BRAF mutational status on expression profiles in conventional papillary thyroid carcinomas. BMC Genomics 2015;16(Suppl 1):S6 View Article PubMed/NCBI
  44. Chen S, Wang Y, Xu M, Zhang L, Su Y, Wang B, et al. miR-1184 regulates the proliferation and apoptosis of colon cancer cells via targeting CSNK2A1. Mol Cell Probes 2020;53:101625 View Article PubMed/NCBI
  45. Di Z, Di M, Fu W, Tang Q, Liu Y, Lei P, et al. Integrated Analysis Identifies a Nine-microRNA Signature Biomarker for Diagnosis and Prognosis in Colorectal Cancer. Front Genet 2020;11:192 View Article PubMed/NCBI
  46. Kupcinskas J, Bruzaite I, Juzenas S, Gyvyte U, Jonaitis L, Kiudelis G, et al. Lack of association between miR-27a, miR-146a, miR-196a-2, miR-492 and miR-608 gene polymorphisms and colorectal cancer. Sci Rep 2014;4:5993 View Article PubMed/NCBI
  47. Kupcinskas J, Wex T, Link A, Leja M, Bruzaite I, Steponaitiene R, et al. Gene polymorphisms of micrornas in Helicobacter pylori-induced high risk atrophic gastritis and gastric cancer. PLoS One 2014;9(1):e87467 View Article PubMed/NCBI
  48. Zheng Y, Liu Y, Wang M, He Q, Xie X, Lu L, et al. Association between miR-492 rs2289030 G>C and susceptibility to Hirschsprung disease in southern Chinese children. J Int Med Res 2020;48(10):300060520961680 View Article PubMed/NCBI
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Association Between miR-492 rs2289030 G>C and Susceptibility to Neuroblastoma in Chinese Children from Jiangsu Province

Wei-Jing Wang, Chun-Lei Zhou, Xin-Xin Zhang, Ye-Mu Zhao, Chang-Mi Deng, Hai-Yan Wu, Zhen-Jian Zhuo, Jing He
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