微小 RNA-26a 调控尖锐湿疣和阴茎鳞状细胞癌中磷酸酶和张力蛋白同源基因的分子机制。
Molecular mechanism of microRNA-26a regulation of phosphatase and tensin homolog gene in condyloma acuminatum and penile squamous cell carcinoma.
机构信息
Department of Dermatology, Taizhou Municipal Hospital, Taizhou, Zhejiang, China.
Department of Urology, Taizhou Municipal Hospital, Taizhou, Zhejiang, China.
出版信息
J Int Med Res. 2021 Jul;49(7):3000605211014379. doi: 10.1177/03000605211014379.
OBJECTIVE
To investigate the expression levels and mechanisms of microRNA (miRNA) 26a (miR-26a) and phosphatase and tensin homolog (PTEN) in patients with human papillomavirus (HPV)-induced condyloma acuminatum (CA) and penile squamous cell carcinoma (PSCC).
METHODS
Thirty-one patients with HPV-positive CA and 28 with HPV-positive PSCC were included in this retrospective, cross-sectional study. PTEN mRNA and miR-26a levels in lesion tissues, blood, and urine were analyzed by quantitative reverse transcription polymerase chain reaction, and PTEN protein was detected by western blot and enzyme-linked immunosorbent assay. Cell proliferation was assessed by MTT assay. The interaction between miR-26a and PTEN was predicted by bioinformatics analysis and confirmed by dual luciferase reporter assay.
RESULTS
PTEN mRNA and protein levels were significantly lower and miR-26a levels were significantly higher in all samples from patients with PSCC compared with the CA group. Bioinformatics analysis and luciferase reporter assay confirmed PTEN as a target gene of miR-26a. Up-regulation of miR-26a significantly increased the proliferation of Penl1 PSCC cells.
CONCLUSIONS
PTEN expression is down-regulated and miR-26a levels are up-regulated in PSCC compared with CA. PTEN is a direct target gene of miR-26a. These results suggest that miR-26a might regulate HPV-positive progression from CA to PSCC through modulating PTEN.
目的
研究微小 RNA（miRNA）26a（miR-26a）和磷酸酶及张力蛋白同源物（PTEN）在人乳头瘤病毒（HPV）诱导的尖锐湿疣（CA）和阴茎鳞状细胞癌（PSCC）患者中的表达水平及机制。
方法
本回顾性、横断面研究纳入了 31 例 HPV 阳性 CA 患者和 28 例 HPV 阳性 PSCC 患者。采用定量逆转录聚合酶链反应分析病变组织、血液和尿液中的 PTEN mRNA 和 miR-26a 水平，采用 Western blot 和酶联免疫吸附试验检测 PTEN 蛋白。通过 MTT 法评估细胞增殖。通过生物信息学分析预测 miR-26a 与 PTEN 之间的相互作用，并通过双荧光素酶报告基因实验进行验证。
结果
与 CA 组相比，PSCC 组所有患者的 PTEN mRNA 和蛋白水平均显著降低，miR-26a 水平均显著升高。生物信息学分析和荧光素酶报告基因实验证实 PTEN 是 miR-26a 的靶基因。上调 miR-26a 可显著增加 Penl1 PSCC 细胞的增殖。
结论
与 CA 相比，PSCC 中 PTEN 表达下调，miR-26a 水平上调。PTEN 是 miR-26a 的直接靶基因。这些结果表明，miR-26a 可能通过调节 PTEN 来调节 HPV 阳性从 CA 向 PSCC 的进展。
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