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MiR-135b improves proliferation and regulates chemotherapy resistance in ovarian cancer
Journal of Molecular Histology ( IF 2.9 ) Pub Date : 2022-07-06 , DOI: 10.1007/s10735-022-10080-y
Jiping Wang 1 , Rongkui Zhang 1 , Bei Zhang 1 , Li Zhang 1 , Wenyan Jiang 1 , Xiaona Liu 2 , Xiumei Duan 2
Affiliation  

MicroRNAs act as regulators in ovarian tumorigenesis and progression by involving different molecular pathways. Here, we examined the role of miR-135b on growth, chemotherapy resistance in OVCAR3 and SKOV3 ovarian cancer cells. MTT assay was performed to examine proliferation. Transwell migration and matrigel invasion assays were used to assess migration and invasion. Caspase-Glo3/7 assay was carried out to evaluate apoptosis. The dual-luciferase reporter assay was performed to validate the putative binding site. Meanwhile, the miR-135b levels in human ovarian cancer tissue were detected by qPCR assay. Overexpression of miR-135b increased growth, and improved migration and invasion in ovarian cancer cells. Meanwhile, overexpression of miR-135b decreased the cisplatin treatment sensitivity in OVCAR3 and SKOV3 cells. The cisplatin-induced apoptosis was decreased by miR-135b. Furthermore, miR-135b could alter epithelial to mesenchymal transition (EMT) associated proteins expression including E-cadherin, N-cadherin, snail and Vimentin in ovarian cancer cells. Further study demonstrated aberrant expression of miR-135b regulated PTEN and p-AKT expression in ovarian cancer cells. The expression level of miR-135b was increased in human ovarian cancer tissue, compared with normal ovary tissue. MiR-135b involves in tumorigenesis and progression in ovarian cancer cells, and might serve as a promising biomarker to predict chemotherapy sensitivity and prognosis in ovarian cancer.



中文翻译:

MiR-135b 改善卵巢癌的增殖并调节化疗耐药性

微小RNA通过涉及不同的分子途径作为卵巢肿瘤发生和进展的调节剂。在这里,我们检查了 miR-135b 对 OVCAR3 和 SKOV3 卵巢癌细胞生长、化疗耐药性的作用。进行MTT测定以检查增殖。Transwell 迁移和基质胶侵袭测定用于评估迁移和侵袭。进行 Caspase-Glo3/7 测定以评估细胞凋亡。进行双荧光素酶报告基因测定以验证推定的结合位点。同时,通过qPCR法检测人卵巢癌组织中的miR-135b水平。miR-135b 的过表达增加了卵巢癌细胞的生长,并改善了卵巢癌细胞的迁移和侵袭。同时,miR-135b 的过表达降低了 OVCAR3 和 SKOV3 细胞中顺铂治疗的敏感性。miR-135b降低了顺铂诱导的细胞凋亡。此外,miR-135b 可以改变卵巢癌细胞中上皮间质转化 (EMT) 相关蛋白的表达,包括 E-cadherin、N-cadherin、snail 和 Vimentin。进一步的研究表明,卵巢癌细胞中 miR-135b 的异常表达调节了 PTEN 和 p-AKT 的表达。与正常卵巢组织相比,人类卵巢癌组织中 miR-135b 的表达水平升高。MiR-135b 参与卵巢癌细胞的肿瘤发生和进展,可能作为预测卵巢癌化疗敏感性和预后的有前途的生物标志物。蜗牛和波形蛋白在卵巢癌细胞中。进一步的研究表明,卵巢癌细胞中 miR-135b 的异常表达调节了 PTEN 和 p-AKT 的表达。与正常卵巢组织相比,人类卵巢癌组织中 miR-135b 的表达水平升高。MiR-135b 参与卵巢癌细胞的肿瘤发生和进展,可能作为预测卵巢癌化疗敏感性和预后的有前途的生物标志物。蜗牛和波形蛋白在卵巢癌细胞中。进一步的研究表明,卵巢癌细胞中 miR-135b 的异常表达调节了 PTEN 和 p-AKT 的表达。与正常卵巢组织相比,人类卵巢癌组织中 miR-135b 的表达水平升高。MiR-135b 参与卵巢癌细胞的肿瘤发生和进展,可能作为预测卵巢癌化疗敏感性和预后的有前途的生物标志物。

更新日期:2022-07-07
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