Xiang Guixian, Cheng Yan
Department of Pharmacology, Xingtai Medical College, Xingtai 054000, China.
Department of Pharmacology, Xingtai Medical College, Xingtai 054000, China.
Reprod Biol. 2018 Sep;18(3):218-224. doi: 10.1016/j.repbio.2018.07.005. Epub 2018 Jul 24.
Ovarian cancer is one of the leading malignancies in women and the 5-year survival rate of ovarian cancer still remains poor. In the present study, we aimed to investigate the interaction between the miR-126-3p and PLXNB2 in the progression of ovarian cancer. The qRT-PCR data revealed a reduction of miR-126-3p level in ovarian cancer tissues comparing to the adjacent normal tissues. Over-expression of miR-126-3p in ovarian cancer cells suppressed cell proliferation and invasion and the phosphorylation of AKT and ERK1/2. The cell cycle assay results showed that the over-expression of miR-126-3p induced cells in G1-phase and reduced cells in S-phase. We further performed bioinformatics analysis and luciferase assay to investigate the relationship between miR-126-3p and PLXNB2 in ovarian cancer cells. The results of TargetScan suggested that PLXNB2 is a direct target of miR-126-3p in ovarian cancer cells, and luciferase assay confirmed bioinformatics prediction. Knocking down of PLXNB2 with PLXNB2 siRNA results in repressed ovarian cancer cell proliferation and invasion, and decreased phosphorylation of AKT and ERK1/2, which is similar to the effect of over-expression of miR-126-3p in OC cells. The synergistic effect of combination of miR-126-3p over-expression and PLXNB2 down-regulation on the cell growth viability, cell colony, and cell invasion was also identified. All these findings indicated that miR-126-3p is involved in the progression of ovarian cancer via direct regulating PLXNB2.
卵巢癌是女性主要的恶性肿瘤之一,其5年生存率仍然很低。在本研究中,我们旨在探讨miR-126-3p与PLXNB2在卵巢癌进展中的相互作用。qRT-PCR数据显示,与相邻正常组织相比,卵巢癌组织中miR-126-3p水平降低。在卵巢癌细胞中过表达miR-126-3p可抑制细胞增殖和侵袭以及AKT和ERK1/2的磷酸化。细胞周期分析结果表明,miR-126-3p的过表达诱导细胞进入G1期并减少S期细胞。我们进一步进行了生物信息学分析和荧光素酶测定,以研究卵巢癌细胞中miR-126-3p与PLXNB2之间的关系。TargetScan的结果表明,PLXNB2是卵巢癌细胞中miR-126-3p的直接靶点,荧光素酶测定证实了生物信息学预测。用PLXNB2 siRNA敲低PLXNB2会导致卵巢癌细胞增殖和侵袭受到抑制,以及AKT和ERK1/2的磷酸化降低,这与在卵巢癌细胞中过表达miR-126-3p的效果相似。还确定了miR-126-3p过表达和PLXNB2下调联合对细胞生长活力、细胞集落和细胞侵袭的协同作用。所有这些发现表明,miR-126-3p通过直接调节PLXNB2参与卵巢癌的进展。