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ATG4B promotescolorectal cancergrowth independent ofautophagic flux Pei‐Feng LiuChung‐Man LeungYu-Hsiang Chang2014 год

ATG4B promotes colorectal cancer growth independent of autophagic flux
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Полный текстСтраница публикацииПубликация в OpenAlex
Аннотация: Autophagy is reported to suppress tumor proliferation, whereas deficiency of autophagy is associated with tumorigenesis. ATG4B is a deubiquitin-like protease that plays dual roles in the core machinery of autophagy; however, little is known about the role of ATG4B on autophagy and proliferation in tumor cells. In this study, we found that ATG4B knockdown induced autophagic flux and reduced CCND1 expression to inhibit G1/S phase transition of cell cycle in colorectal cancer cell lines, indicating functional dominance of ATG4B on autophagy inhibition and tumor proliferation in cancer cells. Interestingly, based on the genetic and pharmacological ablation of autophagy, the growth arrest induced by silencing ATG4B was independent of autophagic flux. Moreover, dephosphorylation of MTOR was involved in reduced CCND1 expression and G1/S phase transition in both cells and xenograft tumors with depletion of ATG4B. Furthermore, ATG4B expression was significantly increased in tumor cells of colorectal cancer patients compared with adjacent normal cells. The elevated expression of ATG4B was highly correlated with CCND1 expression, consistently supporting the notion that ATG4B might contribute to MTOR-CCND1 signaling for G1/S phase transition in colorectal cancer cells. Thus, we report that ATG4B independently plays a role as a positive regulator on tumor proliferation and a negative regulator on autophagy in colorectal cancer cells. These results suggest that ATG4B is a potential biomarker and drug target for cancer therapy.
Год издания: 2014
Авторы: Pei‐Feng Liu, Chung‐Man Leung, Yu-Hsiang Chang, Jin‐Shiung Cheng, Jih‐Jung Chen, Chung-Jeu Weng, Kuo‐Wang Tsai, Chien-Jen Hsu, Yen‐Chen Liu, Ping‐Chi Hsu, Hung‐Wei Pan, Chih‐Wen Shu
Издательство: Taylor & Francis
Источник: Autophagy
Ключевые слова: Autophagy in Disease and Therapy, Epigenetics and DNA Methylation, Endoplasmic Reticulum Stress and Disease
Другие ссылки: Autophagy (PDF)
Autophagy (HTML)
Europe PMC (PubMed Central) (PDF)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
PubMed (HTML)