Ovarian cancer (OC) is one of the most common malignancies of the female reproductive system. The miRNA miR-582-3p is associated with a variety of tumors, and the aim of this study was to investigate the role and mechanisms of miR-582-3p specifically in ovarian carcinogenesis and progression. Low expression of miR-582-3p was noted in OC tissue and cell lines, and lower expression of miR-582-3p correlated with lower overall survival in OC patients. Knockdown of miR-582-3p promoted the proliferation and migration of OC cells, while overexpression inhibited them. TUG1, a long non-coding RNA, was found to bind to miR-582-3p, and inhibition of lncRNA TUG1 decreased viability and migration and weakened the effect of miR-582-3p knockdown in OC cells. Implantation of OC cells with reduced miR-582-3p caused increased tumor growth, while lncRNA TUG1 knockdown suppressed tumor growth and relieved the impact of reduced miR-582-3p
in vivo
. Phosphorylation of AKT and mTOR were significantly enhanced with decreased miR-582-3p expression, but lncRNA TUG1 knockdown attenuated this trend
in vitro
and
in vivo
. The novel miR-582-3p represses the malignant properties of OC
via
the AKT/mTOR signaling pathway by targeting lncRNA TUG1. This axis may represent valuable prognostic biomarkers and therapeutic targets for OC.
The aim of the present study was to investigate the expression of bone morphogenetic protein 7 (BMP7) in cervical cancer tissues, the effect of BMP7 on the proliferation, migration and epithelial-mesenchymal transition (EMT) of cervical cancer HeLa cells and the possible mechanism involved. Immunohistochemistry was used to stain the cervical cancer tissues and benign or precancerous lesions. Lentivirus containing BMP7 knockdown was transfected in HeLa cells and western blotting was performed to analyze BMP7 expression. At the same time, the influence of BMP7 knockdown on the expression of phosphorylated (p)-mothers against decapentaplegic homolog 1/5/9 and EMT-related markers [epithelial-cadherin, neural-cadherin, Vimentin, Snail and Slug] was detected. cell counting Kit-8 was used to detect cell proliferation. Transwell migration and invasion assays were performed to measure cell invasion and migration. The cell cycle was detected by flow cytometry. compared with normal cervical epithelial and paracancerous cells, the positive rate of BMP7 expression in cervical cancer tissues was significantly increased. As compared with the control group, the expression of BMP7 was decreased in HeLa cells transfected with lentivirus. The knockdown of BMP7 in cervical cancer HeLa cells inhibited cell proliferation, migration and invasion, resulted in G1 cell cycle arrest and reversed the EMT process. In addition, the expression of p-Smad1/5/9 was significantly decreased in HeLa cells with BMP7 knockdown. BMP7 is expected to be a possible target for the treatment of cervical cancer.
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