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LncRNA PTENP1 inhibits cervical cancer progression by suppressing miR-106b.
Artificial Cells, Nanomedicine, and Biotechnology ( IF 5.8 ) Pub Date : 2020-01-09 , DOI: 10.1080/21691401.2019.1709852
Yingrui Fan 1 , Weiwei Sheng 1 , Yi Meng 1 , Yundi Cao 1 , Rong Li 1
Affiliation  

LncRNA PTENP1 is a competitive endogenous RNA (ceRNA) involved in decoying miR-106b in multiple diseases. This study investigates the interaction of PTENP1 and miR-106b in cell proliferation, apoptosis and epithelial-mesenchymal transition (EMT) in cervical cancer. The expressions of PTENP1, miR-106b and PTEN were determined in cervical cancer tissues, adjacent normal tissues, cervical cancer cells (HeLa, SiHa, C33A and CasKi) and normal cervical epithelial H8 cells. Up-regulation of PTENP1 and down-regulation of miR-106b were conducted in HeLa and CasKi cells by transfecting cells with corresponding miRNA mimics and inhibitors. Bioinformatics analysis, luciferase reporter assay and RNA-pull down assay were performed to verify the association of miR-106b, PTEN, and PTENP1. Cell growth and cell apoptosis were determined by CCK-8 and flow cytometry analysis. It was found that the expressions of PTENP1 and PTEN were up-regulated and that of miR-106b were down-regulated in cervical cancer tissues and cells. PTENP1 localized in cytoplasm and competitively bound to miR-106b. Up-regulation of PTENP1 and down-regulation of miR-106b contributed to increased expressions of PTEN and E-cadherin. Decreased expression of miR-106b, ZEB1, Snail and Vimentin, resulted in inhibiting cell proliferation and promoting cell apoptosis. Over-expression of PTENP1 and miR-106b accelerated cell proliferation and slowed down cell apoptosis. miR-106b inhibited the expression of PTEN. Our results suggest that LncRNA PTENP1 inhibits cervical cancer progression by competitively binding to miR-106b, leading to promote PTEN expression, inhibit cell proliferation and EMT and induce cell apoptosis in cervical cancer cells.

中文翻译:

LncRNA PTENP1通过抑制miR-106b抑制子宫颈癌的进展。

LncRNA PTENP1是一种竞争性内源RNA(ceRNA),涉及多种疾病中miR-106b的诱变。这项研究调查了PTENP1和miR-106b在宫颈癌的细胞增殖,凋亡和上皮-间质转化(EMT)中的相互作用。在宫颈癌组织,邻近的正常组织,宫颈癌细胞(HeLa,SiHa,C33A和CasKi)和正常宫颈上皮H8细胞中检测PTENP1,miR-106b和PTEN的表达。通过用相应的miRNA模拟物和抑制剂转染细胞,在HeLa和CasKi细胞中进行PTENP1的上调和miR-106b的下调。进行了生物信息学分析,荧光素酶报告基因分析和RNA下拉分析,以验证miR-106b,PTEN和PTENP1的关联。通过CCK-8和流式细胞仪分析确定细胞生长和细胞凋亡。发现在宫颈癌组织和细胞中PTENP1和PTEN的表达上调,而miR-106b的表达下调。PTENP1定位在细胞质中,与miR-106b竞争结合。PTENP1的上调和miR-106b的下调有助于PTEN和E-钙粘蛋白的表达增加。miR-106b,ZEB1,Snail和波形蛋白的表达降低,导致抑制细胞增殖和促进细胞凋亡。PTENP1和miR-106b的过度表达可促进细胞增殖并减缓细胞凋亡。miR-106b抑制PTEN的表达。我们的结果表明,LncRNA PTENP1通过竞争性结合miR-106b抑制宫颈癌的进展,从而促进PTEN表达,
更新日期:2020-12-01
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