Suppr超能文献

Pim-2与下游因子XIAP协同作用,抑制前列腺癌细胞凋亡并增强恶性程度。

Pim-2 Cooperates with Downstream Factor XIAP to Inhibit Apoptosis and Intensify Malignant Grade in Prostate Cancer.

作者信息

Ren Ke, Gou Xin, Xiao Mingzhao, He Weiyang, Kang Jian

机构信息

Department of Urology, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong Distrct, Chongqing, 400016, People's Republic of China.

出版信息

Pathol Oncol Res. 2019 Jan;25(1):341-348. doi: 10.1007/s12253-017-0353-9. Epub 2017 Nov 9.

Abstract

To find the exact downstream effector of Pim-2 pathway in prostate cancer cells, and to determine the means by which it affects prostate cancer. XIAP, Pim-2 and p-eIF4B expressions were detected in PCA and BPH tissues. Then the Pim-2 and XIAP expressions were manipulated using transfection or RNAi in prostatic cells. Finally, Pim-2/eIF4B/XIAP levels were examined in PCA tissues with different clinicopathologic features. XIAP was significantly higher in PCA than in BPH tissues. When Pim-2 was transfected into noncancerous prostate epithelial cells RWPE-1, Pim-2, p-eIF4B and XIAP were all significantly increased and the apoptosis rate was significantly decreased. When XIAP was transfected into RWPE-1 cells, XIAP was significantly increased with no impact on Pim-2, p-eIF4B and the apoptosis rate. When Pim-2 SiRNA was transfected into prostate cancer cells PC-3, Pim-2, p-eIF4B and XIAP were significantly decreased and the apoptosis rate was significantly increased. When XIAP SiRNA was transfected into PC-3 cells, XIAP was significantly decreased with no impact on Pim-2, p-eIF4B and apoptosis rate. Pim-2, p-eIF4B and XIAP were all significantly higher in PCA tissues with GS ≥8 than those with GS ≤7. XIAP is the downstream factor of Pim-2 pathway in prostate cancer cells. Pim-2 and XIAP cooperate in inhibiting the apoptosis of prostate cancer cells. The activation of Pim-2 pathway may predict higher GS in prostate cancer.

摘要

寻找前列腺癌细胞中Pim-2信号通路的确切下游效应分子,并确定其影响前列腺癌的机制。检测前列腺癌(PCA)组织和良性前列腺增生(BPH)组织中XIAP、Pim-2和磷酸化真核细胞起始因子4B(p-eIF4B)的表达。然后在前列腺细胞中通过转染或RNA干扰来调控Pim-2和XIAP的表达。最后,检测具有不同临床病理特征的PCA组织中Pim-2/eIF4B/XIAP的水平。PCA组织中XIAP的表达显著高于BPH组织。将Pim-2转染至非癌性前列腺上皮细胞RWPE-1中时,Pim-2、p-eIF4B和XIAP均显著升高,细胞凋亡率显著降低。将XIAP转染至RWPE-1细胞中时,XIAP显著升高,而对Pim-2、p-eIF4B和细胞凋亡率无影响。将Pim-2小干扰RNA(SiRNA)转染至前列腺癌细胞PC-3中时,Pim-2、p-eIF4B和XIAP显著降低,细胞凋亡率显著升高。将XIAP SiRNA转染至PC-3细胞中时,XIAP显著降低,而对Pim-2、p-eIF4B和细胞凋亡率无影响。在 Gleason评分(GS)≥8的PCA组织中,Pim-2、p-eIF4B和XIAP均显著高于GS≤7的组织。XIAP是前列腺癌细胞中Pim-2信号通路的下游因子。Pim-2和XIAP协同抑制前列腺癌细胞的凋亡。Pim-2信号通路的激活可能预示前列腺癌具有更高的GS。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验