CCDC85C suppresses colorectal cancer cells proliferation and metastasis through activating GSK-3β and promoting β-catenin degradation

Hu, Wenlong; Shen, Jie; Yu, Tao; Dong, Dan Hong; Lu, Sizhao; Li, Liu; Sun, Dongdong; Fan, Ming‐Yu; Chen, Xu; Shen, Weixing; Yu, Caoyang; Cheng, Haibo

doi:10.1016/j.cellsig.2023.110799

Cited by 1 publication

(1 citation statement)

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“…VBP1 stabilizes pVHL by repressing pVHL ubiquitination, which regulates HIF-1α-induced EMT and CRC metastasis by stabilizing pVHL [69]. CCDC85C overexpression promoted β-catenin phosphorylation and ubiquitination by enhancing the functionality of GSK-3β, which thereby serves as a suppressor of CRC cell proliferation and migration [81] (Figure 4).…”

Section: Ubiquitination Regulates Emtmentioning

confidence: 99%

Role of Post-Translational Modifications in Colorectal Cancer Metastasis

Peng,

Liu,

Hai

et al. 2024

Cancers

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Colorectal cancer (CRC) is one of the most common malignant tumors of the digestive tract. CRC metastasis is a multi-step process with various factors involved, including genetic and epigenetic regulations, which turn out to be a serious threat to CRC patients. Post-translational modifications (PTMs) of proteins involve the addition of chemical groups, sugars, or proteins to specific residues, which fine-tunes a protein’s stability, localization, or interactions to orchestrate complicated biological processes. An increasing number of recent studies suggest that dysregulation of PTMs, such as phosphorylation, ubiquitination, and glycosylation, play pivotal roles in the CRC metastasis cascade. Here, we summarized recent advances in the role of post-translational modifications in diverse aspects of CRC metastasis and its detailed molecular mechanisms. Moreover, advances in drugs targeting PTMs and their cooperation with other anti-cancer drugs, which might provide novel targets for CRC treatment and improve therapeutic efficacy, were also discussed.

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Section: Ubiquitination Regulates Emtmentioning

confidence: 99%