Are cachexia-associated tumors transmitTERS of ER stress?

Autor(es)

Yamagata, Ana Sayuri ^[1] ; Freire, Paula Paccielli ^[2]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Cell & Dev Biol, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, Sao Paulo - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: BIOCHEMICAL SOCIETY TRANSACTIONS; v. 49, n. 4, p. 1841-1853, AUG 2021.
• Citações Web of Science: 1

Resumo

Cancer cachexia is associated with deficient response to chemotherapy. On the other hand, the tumors of cachectic patients remarkably express more chemokines and have higher immune infiltration. For immunogenicity, a strong induction of the unfolded protein response (UPR) is necessary. UPR followed by cell surface exposure of calreticulin on the dying tumor cell is essential for its engulfment by macrophages and dendritic cells. However, some tumor cells upon endoplasmic reticulum (ER) stress can release factors that induce ER stress to other cells, in the so-called transmissible ER stress (TERS). The cells that received TERS produce more interleukin 6 (IL-6) and chemokines and acquire resistance to subsequent ER stress, nutrient deprivation, and genotoxic stress. Since ER stress enhances the release of extracellular vesicles (EVs), we suggest they can mediate TERS. It was found that ER stressed cachexia-inducing tumor cells transmit factors that trigger ER stress in other cells. Therefore, considering the role of EVs in cancer cachexia, the release of exosomes can possibly play a role in the process of blunting the immunogenicity of the cachexia-associated tumors. We propose that TERS can cause an inflammatory and immunosuppressive phenotype in cachexia-inducing tumors. (AU)

• Processo FAPESP: 20/00086-6 - Proteostase no tecido adiposo de pacientes com Caquexia associada ao Câncer
• Beneficiário: Ana Sayuri Yamagata
• Modalidade de apoio: Bolsas no Brasil - Doutorado Direto
• Processo FAPESP: 12/11666-7 - Cinética da expressão de micro-RNAs músculo específicos miR-208 e miR-499 em células tratadas in vitro com TNF-alfa e INF-gama
• Beneficiário: Paula Paccielli Freire-Barguil
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica