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Vimentin loss promotes cancer proliferation through up-regulating Rictor/AKT/β-catenin signaling pathway

Ding, Youxiang, Lv, Conggai, Zhou, You, Zhang, Heng, Zhao, Li, Xu, Yuting, Fan, Xiangshan·2021·Experimental Cell Research
DOI 10.1016/j.yexcr.2021.112666
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Abstract

Vimentin protein is one of the main cytoskeleton and plays an important role in cell motility and metastasis. Nowadays, vimentin is widely studied as an epithelial-mesenchymal transition (EMT) marker of cancer cells while its involvement in cancer proliferation is poorly understood. In this study, we investigated the participation of vimentin in regulating cancer proliferation by silencing VIM gene in four cancer cell lines. Our results demonstrated that vimentin loss significantly induced cancer cell proliferation both in vitro and in vivo, which has not been reported so far. Mechanistically, knockdown of vimentin expression activated AKT phosphorylation and its downstream β-catenin signaling. Nuclear translocation and transcriptional activity of β-catenin was enhanced after silencing vimentin expression. Furthermore, vimentin loss could prevent Rictor from autophagy-dependent degradation via reducing AMPK-mediated autophagy signaling. AICAR, an AMPK activator, down-regulated Rictor and p-AKT levels while vimentin knockdown could rescue the effects. In vivo, it was also found that Ki67 expression and p-AKT/β-catenin signaling pathway were obviously up-regulated in the tumor tissues in which vimentin was silenced compared to control groups. Taken together, these data showed the novel function of vimentin in regulating cancer proliferation via Rictor/AKT/β-catenin signaling pathway, which suggested that it need more careful consideration before inhibiting metastatic cancers th…

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Metadata

Authors
Ding, Y., Lv, C., Zhou, Y., Zhang, H., Zhao, L., Xu, Y., & Fan, X.
Venue
Experimental Cell Research
Publisher
Elsevier BV
Published
2021-08
Volume
405
Issue
1
Pages
112666
ISSN
0014-4827
DOI
10.1016/j.yexcr.2021.112666
Cited by
21
References
0
Language
en
Licence
Funders
  • National Natural Science Foundation of China (81773774)
  • China Pharmaceutical University (CPU2018GY37)
  • Double First Class University Plan

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