Mortalin contributes to colorectal cancer by promoting proliferation and epithelial-mesenchymal transition
Mortalin contributes to colorectal cancer by promoting proliferation and epithelial-mesenchymal transition
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Mortalin 通过促进增殖和上皮间质转化而导致结直肠癌
DOI：
10.1002/iub.2176
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发表时间：
2020-04-01
期刊：
影响因子：
4.6
通讯作者：
Lin, Zhenhua
中科院分区：
文献类型：
--
作者：
Xu, Ming;Zhang, Yuan;Lin, Zhenhua
本研究旨在探讨mortalin在结直肠癌（CRC）中的表达。Mortalin激活Wnt/ β -连环蛋白通路，加速细胞增殖和上皮-间质转化（EMT）程序。来自在线数据库的数据显示，mortalin在CRC中的表达较高，这一点在临床标本中得到了进一步的验证。同时，高死亡率表达与较差的总生存率呈正相关。通过3-（4,5-二甲基-2-噻唑基）-2,5-二苯基-2- h -溴化四氮唑（MTT）、菌落形成和免疫荧光染色试验评估，抑制莫他林可抑制结直肠癌细胞增殖。此外，mortalin的缺失抑制了CRC细胞EMT的进展，并使Wnt/ β -catenin通路失活。总之，mortalin在结直肠癌中高表达，可能预示预后不良。死亡素通过刺激细胞增殖和EMT程序加速结直肠癌的进展。本研究可能为结直肠癌提供一个潜在的临床治疗靶点。
This study focused on the expression of mortalin in colorectal cancer (CRC). Mortalin activated the Wnt/beta-catenin pathway to accelerate cell proliferation and the epithelial-mesenchymal transition (EMT) program. Data from online databases displayed that the expression of mortalin was high in CRC, which was further validated using clinical specimens. Meanwhile, high mortalin expression was positively associated with a poor overall survival rate. Suppression of mortalin inhibited CRC cell proliferation as evaluated by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, and immunofluorescence staining assays. In addition, depletion of mortalin inhibited CRC cell EMT progression and deactivated the Wnt/beta-catenin pathway. Altogether, mortalin is highly expressed in CRC and may indicate a poor prognosis. Mortalin accelerated CRC progression by stimulating cell proliferation and the EMT program. This study may provide a potential clinical therapeutic target for CRC.