ArticleCell cycle (Georgetown, Tex.)2019
A novel function of anaphase promoting complex subunit 10 in tumor progression in non-small cell lung cancer.
Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- SUCLG2 contributes to platinum resistance in lung adenocarcinoma through enhancing succinylation of GAC and glutamine metabolism.Apoptosis : an international journal on programmed cell death · 2026Article
- The APC/C subunit APC7 promotes hepatocellular carcinoma progression by mediating ubiquitination and degradation of LATS1 to activate YAP/TAZ.Biology direct · 2026Article
- Recombinant α-Toxin BmK-M9 Inhibits Breast Cancer Progression by Regulating β-Catenin In Vivo.Cell biochemistry and biophysics · 2025Article
- ANAPC10 expression predicts poor prognosis in oral squamous cell carcinoma and promotes tumor growth via the PI3K/AKT/mTOR pathway.Discover oncology · 2025Article
- Searching for a Putative Mechanism of RIZ2 Tumor-Promoting Function in Cancer Models.Frontiers in oncology · 2020Article
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10 authors.
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Abstract
The anaphase promoting complex/cyclosome (APC/C), a cell cycle-regulated E3 ubiquitin ligase, is responsible for the transition from metaphase to anaphase and the exit from mitosis. The anaphase promoting complex subunit 10 (APC10), a subunit of the APC/C, executes a vital function in substrate recognition. However, no research has reported the connection between APC10 and cancer until now. In this study, we uncovered a novel, unprecedented role of APC10 in tumor progression, which is independent of APC/C. First, aberrant increase of APC10 expression was validated in non-small cell lung cancer (NSCLC) cells and tissues, and the absence of APC10 repressed cell proliferation and migration. Of great interest, we found that APC10 inhibition induced cell cycle arrest at the G0/G1 phase and reduced the expression of the APC/C substrate, Cyclin B1; this finding is different from the conventional concept of the accumulation of Cyclin B1 and cell cycle arrest in metaphase. Further, APC10 was found to interact with glutaminase C (GAC), and the inhibition of APC10 weakened glutamine metabolism and induced excessive autophagy. Taken together, these findings identify a novel function of APC10 in the regulation of NSCLC tumorigenesis and point to the possibility of APC10 as a new target for cancer therapy.
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