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The Role of STAT3 Polymorphism in the Development of Cervical Cancer Caused by HPV16 |
ZHANG Hemin, YU Yan, LIU Yanyun |
Cangshan Branch of the 900th Hospital of the Joint Logistic Support Force, Fujian Fuzhou 350000, China |
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Abstract Objective: To investigate the role of signal transducer and activator of transcription 3 (STAT3) polymorphism in the development of cervical cancer caused by human papillomavirus 16 (HPV16). Methods: A retrospective study was conducted on 34 patients with cervical cancer who were admitted to the hospital from 2019 to 2023. They were assigned to Group A. Another 54 patients with cervical intraepithelial neoplasia and 80 patients with chronic cervicitis admitted to the hospital during the same period were assigned to Groups B and C, respectively. The expression of HPV16 E6 protein was detected by immunohistochemistry and polymerase chain reaction (PCR)-reverse dot blot hybridization. The expression of STAT3 protein was detected by PCR, and the polymorphism of STAT3 gene C1697G was detected by PCR-restriction fragment length polymorphism (RFLP). The expression rates of E6 and STAT3 proteins and the genotypes of STAT3 gene polymorphism in the three groups were compared and analyzed. Results: The positive expression rates of E6 and STAT3 proteins in Group A were significantly higher than those in Groups B and C (P<0.0167). The positive expression rates of E6 and STAT3 proteins in Group B were significantly higher than those in Group C (P<0.0167). The frequency of the G/G genotype in Groups A and B was significantly lower than that in Group C, and the frequency of the C/C genotype was significantly higher than that in Group C (P<0.0167). The frequency of the G/G genotype in Group A was significantly lower than that in Group B, and the frequency of the C/C genotype was significantly higher than that in Group B (P<0.0167). There was no significant difference in the frequency of the G/C genotype among the three groups (P>0.0167). Conclusion: STAT3 and its polymorphism may play an important role in the development and progression of cervical cancer caused by HPV16.
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[1] 雷声云,吕海利,郑春艳.STAT3基因多态性与女性人乳头瘤病毒感染及宫颈病变的关系[J].中国微生态学杂志,2021,33(11):1313-1316,1325. [2] 范怡冰.宫颈分泌物中Stat3和Survivin的测定在宫颈病变筛查中的价值[J].中国妇幼健康研究,2018,29(9):1123-1128. [3] 刘琳,沈攀,张力忆,等.宫颈病变内高危型HPV感染与Th细胞分化、细胞异常增殖的相关性[J].海南医学院学报,2018,24(3):315-318. [4] 莫小亮,覃桂荣,蒋晓莉,等.STAT3及其多态性在HPV16所致宫颈癌发生过程中的作用研究[J].中国当代医药,2021,28(1):16-19,26. [5] 谢幸,孔北华,段涛.妇产科学[M].第9版.北京:人民卫生出版社,2018.278-279. [6] 张梦,马冬,袁腾,等.miR-135a-5p、GATA3和STAT3在宫颈癌中的表达及其相关性[J].肿瘤防治研究,2019,46(4):338-344. [7] Gauri S,Gaurav V,Yogesh S,et al.Deregulation of microRNAs Let-7a and miR-21 mediate aberrant STAT3 signaling during human papillomavirus-induced cervical carcinogenesis:role of E6 oncoprotein[J].BMC Cancer,2019,14(6):635-642. [8] 张英,邓丽娜,徐传彬.STAT3基因多态性与HPV感染及宫颈病变的关系[J].检验医学与临床,2017,14(21):3211-3213. [9] Lin W,Bowen S,Junpeng L,et al.STAT3 exerts pro-tumor and anti-autophagy roles in cervical cancer[J].Diagnostic Pathology,2022,17(1):258-264. [10] Adrian K,Antons M,Lugo N S,et al.STAT3 is a potential therapeutic target in cervical cancer (257)[J].Gynecologic Oncology,2022,166(11):259-265. [11] 张慧蓉,申东翔,罗敏,等.STAT3 对宫颈癌HeLa细胞的增殖、凋亡及自噬的影响[J].实用医学杂志,2018,34(16):2653-2658. [12] 高和平,朱姗姗,徐福霞,等.STAT3在HPV16/18相关宫颈癌中的致病机制研究[J].中国优生与遗传杂志,2021,29(8):1083-1087. |
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