The Role of Chaperone-Mediated Autophagy in Cell Cycle Control and Its Implications in Cancer

Autor(es)

Andrade-Tomaz, Marina ^[1] ; de Souza, Izadora ^[1] ; Ribeiro Reily Rocha, Clarissa ^[1] ; Rodrigues Gomes, Luciana ^[2]

Afiliação do(s) autor(es)

^[1] Univ Fed Sao Paulo, Dept Oncol Clin & Expt, Escola Paulista Med, BR-04037003 Sao Paulo, SP - Brazil

^[2] Inst Butantan, Ctr Toxins Immune Response & Cell Signaling CeTIC, Lab Ciclo Celular, BR-05503001 Sao Paulo, SP - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: CELLS; v. 9, n. 9 SEP 2020.
• Citações Web of Science: 0

Resumo

The cell cycle involves a network of proteins that modulate the sequence and timing of proliferation events. Unregulated proliferation is the most fundamental hallmark of cancer; thus, changes in cell cycle control are at the heart of malignant transformation processes. Several cellular processes can interfere with the cell cycle, including autophagy, the catabolic pathway involved in degradation of intracellular constituents in lysosomes. According to the mechanism used to deliver cargo to the lysosome, autophagy can be classified as macroautophagy (MA), microautophagy (MI), or chaperone-mediated autophagy (CMA). Distinct from other autophagy types, CMA substrates are selectively recognized by a cytosolic chaperone, one-by-one, and then addressed for degradation in lysosomes. The function of MA in cell cycle control, and its influence in cancer progression, are already well-established. However, regulation of the cell cycle by CMA, in the context of tumorigenesis, has not been fully addressed. This review aims to present and debate the molecular mechanisms by which CMA can interfere in the cell cycle, in the context of cancer. Thus, cell cycle modulators, such as MYC, hypoxia-inducible factor-1 subunit alpha (HIF-1 alpha), and checkpoint kinase 1 (CHK1), regulated by CMA activity will be discussed. Finally, the review will focus on how CMA dysfunction may impact the cell cycle, and as consequence promote tumorigenesis. (AU)

• Processo FAPESP: 13/07467-1 - CeTICS - Centro de Toxinas, Imuno-Resposta e Sinalização Celular
• Beneficiário: Hugo Aguirre Armelin
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
• Processo FAPESP: 19/21745-0 - Explorando mecanismos de resistência a quimioterápicos em células de câncer via bibliotecas CRISPR
• Beneficiário: Clarissa Ribeiro Reily Rocha
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 19/19435-3 - Papel de danos no DNA e função mitocondrial em envelhecimento vascular, imune e neurológico (DNA MoVINg)
• Beneficiário: Carlos Frederico Martins Menck
• Modalidade de apoio: Auxílio à Pesquisa - Temático