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PlncRNA-1 induces apoptosis through the Her-2 pathway in prostate cancer cells

机译:PlncRNA-1通过Her-2途径诱导前列腺癌细胞凋亡

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摘要

To determine whether PlncRNA-1 induces apoptosis in prostate cancer cells through the Her-2 pathway. The expression of PlncRNA-1, Her-2, and related cyclin proteins in 23 cases of prostate cancer and adjacent normal tissues was analyzed and compared. LNCaP cells were divided into a control group and an LNCaP-PlncRNA-1-siRNA experimental group. Normal prostate RWPE-1 cells were divided into an RWPE-1 control group and an RWPE-1-PlncRNA-1 experimental group. After PlncRNA-1 silencing and overexpression, changes in Her-2 and cyclinD1 expression levels were detected both in vivo and in vitro. In prostate cancer tissues, Her-2 and PlncRNA-1 were highly expressed and significantly correlated. In LNCaP cells, the expression of Her-2 and cyclinD1 decreased following the downregulation of PlncRNA-1 as assessed by real-time PCR and Western blotting. In RWPE-1 cells, the expression of Her-2 and cyclinD1 increased following PlncRNA-1 overexpression. Flow cytometry revealed that the proportion of LNCaP cells in G2/M phase was significantly increased after PlncRNA-1 silencing and that the proportion of RWPE-1 cells in G2/M phase was significantly decreased after PlncRNA-1 overexpression. Furthermore, animal experiments validated these results. In conclusion, in prostate cancer, PlncRNA-1 regulates the cell cycle and cyclinD1 levels and can also regulate proliferation and apoptosis in prostate cancer cells through the Her-2 pathway.
机译:确定PlncRNA-1是否通过Her-2途径诱导前列腺癌细胞凋亡。分析和比较了23例前列腺癌和邻近正常组织中PlncRNA-1,Her-2和相关细胞周期蛋白的表达。将LNCaP细胞分为对照组和LNCaP-PlncRNA-1-siRNA实验组。正常前列腺RWPE-1细胞分为RWPE-1对照组和RWPE-1-PlncRNA-1实验组。在PlncRNA-1沉默和过表达后,在体内和体外均检测到Her-2和cyclinD1表达水平的变化。在前列腺癌组织中,Her-2和PlncRNA-1高度表达并显着相关。在LNCaP细胞中,通过实时PCR和Western印迹评估,PlncRNA-1的下调后Her-2和cyclinD1的表达下降。在RWPE-1细胞中,PlncRNA-1过表达后,Her-2和cyclinD1的表达增加。流式细胞仪显示,PlncRNA-1沉默后,L2 / a期的LNCaP细胞比例显着增加,PlncRNA-1过表达后,G2 / M期的RWPE-1细胞比例显着降低。此外,动物实验验证了这些结果。总之,在前列腺癌中,PlncRNA-1调节细胞周期和cyclinD1水平,还可以通过Her-2途径调节前列腺癌细胞的增殖和凋亡。

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