Regulation of autophagy by Rab27B in colorectal cancer.

Autor: Afroz S; Department of Molecular Biosciences, University of Kansas, Lawrence, KS, USA., Preet R; Department of Molecular Biosciences, University of Kansas, Lawrence, KS, USA., Vishwakarma V; Department of Molecular Biosciences, University of Kansas, Lawrence, KS, USA., Evans AE; Department of Molecular Biosciences, University of Kansas, Lawrence, KS, USA., Magstadt AN; Department of Molecular Biosciences, University of Kansas, Lawrence, KS, USA., Dixon DA; Department of Molecular Biosciences, University of Kansas, Lawrence, KS, USA; University of Kansas Cancer Center, Kansas City, KS, USA. Electronic address: ddixon2@uams.edu.
Jazyk: angličtina
Zdroj: The international journal of biochemistry & cell biology [Int J Biochem Cell Biol] 2024 Nov 13; Vol. 177, pp. 106693. Date of Electronic Publication: 2024 Nov 13.
DOI: 10.1016/j.biocel.2024.106693
Abstrakt: Autophagy is a cellular recycling process that is associated with tumor growth, anti-tumor immune responses, and therapy resistance in colorectal cancer (CRC). In this report, we identify the small GTPase Rab27B to control the autophagy process in CRC. Depletion of Rab27B showed an abnormal accumulation of autophagy vesicles and increased autophagy markers in CRC cells, indicating autophagy dysregulation. Image analysis indicated that autophagy flux is blocked at the autophagosome/lysosome fusion step when Rab27B is lost. While Rab27B deficient cells are proficient at growth under 2D in vitro conditions, cell growth was significantly impacted in both in vitro 3D growth and in vivo tumorigenesis studies. Together, these results demonstrate a new role of Rab27B in the autophagy trafficking process in CRC and identify Rab27B as a potential therapeutic target for CRC.
Competing Interests: Declaration of Competing Interest The authors declare no competing interests.
(Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)
Databáze: MEDLINE
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