miR-221-induced PUMA silencing mediates immune evasion of bladder cancer cells
miR-221-induced PUMA silencing mediates immune evasion of bladder cancer cells
复制标题
miR-221诱导的PUMA沉默介导膀胱癌细胞的免疫逃避
DOI：
10.3892/ijo.2015.2837
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发表时间：
2015-03-01
影响因子：
5.2
通讯作者：
Wang, Gongxian
中科院分区：
文献类型：
--
作者：
Fu, Bin;Wang, Yibing;Wang, Gongxian
肿瘤细胞的免疫逃逸主要是由于免疫细胞对癌细胞的凋亡信号转导受阻，以及随后癌细胞内的凋亡信号级联受到抑制。在过去的几十年里，研究更多地集中在免疫细胞到癌细胞的凋亡信号转导受损，而不是对细胞内信号通路的抑制。本研究将miR-221抑制剂导入膀胱癌5637、J82和T24细胞，以抑制miR-221的表达。结果，miR-221对P53上调的凋亡调节因子(PUMA)的抑制作用被取消，导致促凋亡的Bax表达增加，抗凋亡的Bcl-2表达降低，从而促进膀胱癌细胞的凋亡。MMP2、MMP9和VEGFC的表达减少，从而降低了膀胱癌细胞的侵袭力和侵袭能力，从而抑制了膀胱癌细胞的免疫逃逸。
Immune evasion of cancer cells is mainly due to the impaired transduction of apoptotic signals from immune cells to cancer cells, as well as inhibition of subsequent apoptosis signal cascades within the cancer cells. Over the past few decades, the research has focused more on the impaired transduction of the apoptotic signal from immune cells to cancer cells, rather than inhibition of the intracellular signaling pathways. In this study, miR-221 inhibitor was transfected into bladder cancer cell lines 5637, J82 and T24 to repress the expression of miR-221. As a result, the repression of miR-221 on p53 upregulated modulator of apoptosis (PUMA) was abolished, resulting in increased expression of the pro-apoptotic Bax and reduced expression of the anti-apoptotic Bcl-2, which promotes apoptosis of bladder cancer cells. The expression of MMP-2, MMP-9 and VEGF-C were reduced, resulting in reduced invasiveness and infiltration capability of bladder cancer cells, thereby inhibiting the immune evasion of bladder cancer cells.