目前,研究了许多长链非编码RNA(lncRNA)作为肿瘤抑制因子在宫颈癌(CC)形成和发展中的作用.然而,lncRNA前列腺癌基因表达标志物1(PCGEM1),高表达不仅可加重卵巢癌的发生,还可诱导肿瘤的发生和子宫内膜癌的进展,在CC中没有研究过。本研究的目的是研究PCGEM1在CC中的表达和潜在作用。通过实时PCR检测PCGEM1在CC细胞中的相对表达。shRNA抑制PCGEM1表达后,扩散的变化,迁移,并通过CCK-8测定检测侵袭能力,EdU分析,和集落形成试验伤口愈合试验。通过蛋白质印迹和免疫荧光测定Transwell测定和上皮-间质转化(EMT)标志物的表达变化。PCGEM1,miR-642a-5p,和驱动蛋白家族成员5B(KIF5B)通过生物信息学分析和荧光素酶报告基因测定得到证实。结果显示PCGEM1在CC细胞内表达上调。细胞活力,迁移,shRNA抑制Hela和SiHa细胞中PCGEM1的表达后,侵袭能力明显降低。N-钙黏着蛋白被沉默了,但sh-PCGEM1升高了E-cadherin的表达。此外,通过在CC中使用miR-642a-5p,PCGEM1被证实为调节KIF5B水平的竞争性内源性RNA(ceRNA)。MiR-642a-5p下调部分挽救了sh-PCGEM1对细胞增殖的抑制作用,迁移,入侵,和EMT流程。总之,PCGEM1/miR-642a-5p/KIF5B信号轴可能是CC的新治疗靶点.本研究为CC的靶向治疗提供了研究基础和新方向。
At present, the role of many long non-coding RNAs (lncRNAs) as tumor suppressors in the formation and development of cervical cancer (CC) has been studied. However, lncRNA prostate cancer gene expression marker 1 (PCGEM1), whose high expression not only aggravates ovarian cancer but also can induce tumorigenesis and endometrial cancer progression, has not been studied in CC. The objective of this study was to investigate the expression and the underlying role of PCGEM1 in CC. The relative expression of PCGEM1 in CC cells was detected by real-time PCR. After the suppression of PCGEM1 expression by shRNA, the changes in the proliferation, migration, and invasion capacities were detected via CCK-8 assay, EdU assay, and colony formation assay wound healing assay. Transwell assay and the changes in expressions of epithelial-to-mesenchymal transition (EMT) markers were determined by western blot and immunofluorescence. The interplay among PCGEM1, miR-642a-5p, and kinesin family member 5B (KIF5B) was confirmed by bioinformatics analyses and luciferase reporter assay. Results showed that PCGEM1 expressions were up-regulated within CC cells. Cell viabilities, migration, and invasion were remarkably reduced after the suppression of PCGEM1 expression by shRNA in Hela and SiHa cells. N-cadherin was silenced, but E-cadherin expression was elevated by sh-PCGEM1. Moreover, by sponging miR-642a-5p in CC, PCGEM1 was verified as a competitive endogenous RNA (ceRNA) that modulates KIF5B levels. MiR-642a-5p down-regulation partially rescued sh-PCGEM1\'s inhibitory effects on cell proliferation, migration, invasion, and EMT process. In conclusion, the PCGEM1/miR-642a-5p/KIF5B signaling axis might be a novel therapeutic target in CC. This study provides a research basis and new direction for targeted therapy of CC.