Association between STAT3 rs1053004 polymorphism and cancer risk: a meta-analysis

Document Type : Original article

Authors

1 Department of Clinical Biochemistry, Iranshahr University of Medical Sciences, Iranshahr, Iran

2 Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran

Abstract

Several studies examined the relationship between STAT3 rs1053004 polymorphism and the risk of some human cancers, but the findings remains inconclusive. To evaluate the impact of STAT3 rs1053004 on cancer risk, we conducted a meta-analysis of all available studies including 4,605 cancer cases and 5,248 controls. Eligible studies were identified by searching PubMed, Web of Science, Scopus, and Google scholar databases. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated in codominant, dominant, recessive, overdominant, and allele models to quantitatively estimate the association. The overall findings showed no significant association between STAT3 rs1053004 polymorphism and cancer risk in codominant, dominant, recessive, overdominant, and allele inheritance model tested. In summary, the findings of this meta-analysis indicates no significant association between STAT3 rs1053004 polymorphism and cancer development. Larger and well-designed studies are necessary to estimate this association in detail.


Keywords

References

1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. CA Cancer J Clin 2016;66:7-30.
2. Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, Parkin DM, Forman D, Bray F. Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer 2015;136:E359-386.
3. Foulkes WD. Inherited susceptibility to common cancers. N Engl J Med 2008;359:2143-2153.
4. Hashemi M, Bahari G, Markowski J, Malecki A, Los MJ, Ghavami S. Association of PDCD6 polymorphisms with the risk of cancer: Evidence from a meta-analysis. Oncotarget 2018;9: 24857-24868.
5. Raz R, Durbin JE, Levy DE. Acute phase response factor and additional members of the interferon-stimulated gene factor 3 family integrate diverse signals from cytokines, interferons, and growth factors. J Biol Chem 1994;269:24391-24395.
6. Choi JY, Li WL, Kouri RE, Yu J, Kao FT, Ruano G. Assignment of the acute phase response factor (APRF) gene to 17q21 by microdissection clone sequencing and fluorescence in situ hybridization of a P1 clone. Genomics 1996;37:264-265.
7. Darnell JE, Jr. STATs and gene regulation. Science 1997;277:1630-1635.
8. Galoczova M, Coates P, Vojtesek B. STAT3, stem cells, cancer stem cells and p63. Cell Mol Biol Lett 2018;23:12.
9. Yan R, Lin F, Hu C, Tong S. Association between STAT3 polymorphisms and cancer risk: a meta-analysis. Molecular genetics and genomics 2015;290:2261-2270.
10. Chanthra N, Payungporn S, Chuaypen N, Pinjaroen N, Poovorawan Y, Tangkijvanich P. Association of single nucleotide polymorphism rs1053004 in signal transducer and activator of transcription 3 (STAT3) with susceptibility to hepatocellular carcinoma in Thai patients with chronic hepatitis B. Asian Pac J Cancer Prev 2015;16:5069-5073.
11. Fatemipour M, Arab Zadeh SAM, Molaei H, Geramizadeh B, Fatemipour B, Vahedi SM, Malekpourafshar R. Study on the relationship of demographic characteristics of rs1053004 in STAT3 gene in pationts with HCC following chronic HBV infection. Iran J Virol 2016;10:40-47.
12. Li M, Li F, Li N, Sang J, Fan X, Deng H, Zhang X, Han Q, Lv Y, Liu Z. Association of polymorphism rs1053005 in STAT3 with chronic hepatitis B virus infection in Han Chinese population. BMC Med Genet 2018;19:52.
13. Xie J, Zhang Y, Zhang Q, Han Y, Yin J, Pu R, Shen Q, Lu W, Du Y, Zhao J, Han X, Zhang H, Cao G. Interaction of signal transducer and activator of transcription 3 polymorphisms with hepatitis B virus mutations in hepatocellular carcinoma. Hepatology 2013;57:2369-2377.
14. Zhou F, Cheng L, Qiu L-X, Wang M-Y, Li J, Sun M-H, Yang Y-J, Wang J-C, Jin L, Wang Y-N. Associations of potentially functional variants in IL-6, JAKs and STAT3 with gastric cancer risk in an eastern Chinese population. Oncotarget 2016;7:28112.
15. Zhu B, Zhu Y, Lou J, Ke J, Zhang Y, Li J, Gong Y, Yang Y, Tian J, Peng X, Zou D, Zhong R, Gong J, Chang J, Li L, Miao X. A single nucleotide polymorphism in the 3'-UTR of STAT3 regulates its expression and reduces risk of pancreatic cancer in a Chinese population. Oncotarget 2016;7:62305-62311.
16. Jiang B, Zhu Z, Liu F, Yang L, Zhang W, Yuan H, Wang J, Hu X, Huang G. STAT3 gene polymorphisms and susceptibility to non-small cell lung cancer. Genet Mol Res 2011;10: 1856-1865.
17. Khanna P, Chua PJ, Bay BH, Baeg GH. The JAK/STAT signaling cascade in gastric carcinoma (Review). Int J Oncol 2015;47:1617-1626.
18. Zhong Z, Wen Z, Darnell JE, Jr. Stat3: a STAT family member activated by tyrosine phosphorylation in response to epidermal growth factor and interleukin-6. Science 1994; 264:5-98.
19. Darnell JE, Jr., Kerr IM, Stark GR. Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins. Science 1994;264:1415-1421.
20. Li W, Lee MR, Kim T, Kim YW, Cho MY. Activated STAT3 may participate in tumor progression through increasing CD133/survivin expression in early stage of colon cancer. Biochem Biophys Res Commun 2018;497:354-361.
21. To KF, Chan MW, Leung WK, Ng EK, Yu J, Bai AH, Lo AW, Chu SH, Tong JH, Lo KW, Sung JJ, Chan FK. Constitutional activation of IL-6-mediated JAK/STAT pathway through hypermethylation of SOCS-1 in human gastric cancer cell line. Br J Cancer 2004;91:1335-1341.

Files

Share

How to cite

Statistics