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目的:探讨miR-17-5p在口腔鳞癌发病中的作用和作用机制。方法:收集42例手术后病理诊断为口腔鳞癌(OSCC)组织标本,使用q RT-PCR测定miR-17-5p的表达;通过MTT实验、报告基因实验和Pearson相关性检验探讨miR-17-5p对OSCC的作用和调控机制。结果:在OSCC中miR-17-5p表达显著上调(P<0.05);MTT证实miR-17-5p可以促进肿瘤细胞增殖;报告基因实验证实,细胞因子信号抑制物-6(SOCS6)3’UTR区域存在一个miR-17-5p的结合位点,miR-17-5p通过该结合位点抑制SOCS6的m RNA水平和蛋白水平,进而促进细胞增殖;临床证实miR-17-5p与SOCS6表达呈明显负相关。结论:miR-17-5p在OSCC中表达明显上调,可能通过抑制其下游靶基因SOCS6参与了肿瘤的发生发展。
Objective: To investigate the role and mechanism of miR-17-5p in the pathogenesis of oral squamous cell carcinoma. Methods: Forty-two OSCC specimens were collected for histopathological diagnosis of OSCC. QRT-PCR was used to detect the expression of miR-17-5p. MTT assay, reporter gene assay and Pearson correlation test were used to investigate the expression of miR-17- 5p on the role of OSCC and regulatory mechanisms. Results: The expression of miR-17-5p was significantly upregulated in OSCC (P <0.05). MTT confirmed that miR-17-5p promoted the proliferation of tumor cells. The reporter gene assay confirmed that cytosolic signaling inhibitor-6 (SOCS6) 3’UTR There is a binding site of miR-17-5p in the region, and miR-17-5p inhibits SOCS6 m RNA and protein levels through this binding site, thereby further promoting cell proliferation. The clinical demonstration of miR-17-5p and SOCS6 expression was significant Negative correlation. Conclusion: The expression of miR-17-5p is up-regulated in OSCC, which may be involved in tumor development by inhibiting its downstream target gene SOCS6.