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Mechanisms of cellular crosstalk in the gastric tumor microenvironment are mediated by YAP1 and STAT3.
Thilakasiri, Pathum; O'Keefe, Ryan N; To, Sarah Q; Chisanga, David; Eissmann, Moritz F; Carli, Annalisa LE; Duscio, Belinda; Baloyan, David; Dmello, Rhynelle S; Williams, David; Mariadason, John; Poh, Ashleigh R; Pal, Bhupinder; Kile, Benjamin T; Vissers, Joseph Ha; Harvey, Kieran F; Buchert, Michael; Shi, Wei; Ernst, Matthias; Chand, Ashwini L.
Afiliação
  • Thilakasiri P; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • O'Keefe RN; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • To SQ; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Chisanga D; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Eissmann MF; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Carli AL; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Duscio B; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Baloyan D; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Dmello RS; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Williams D; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Mariadason J; Department of Pathology, Austin Health, Heidelberg, Australia.
  • Poh AR; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Pal B; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Kile BT; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Vissers JH; Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
  • Harvey KF; Peter MacCallum Cancer Centre, Melbourne, Australia.
  • Buchert M; Peter MacCallum Cancer Centre, Melbourne, Australia.
  • Shi W; Department of Anatomy and Developmental Biology, and Biomedicine Discovery Institute, Monash University, Clayton, Australia.
  • Ernst M; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
  • Chand AL; Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia.
Life Sci Alliance ; 7(2)2024 02.
Article em En | MEDLINE | ID: mdl-37957015
ABSTRACT
Deregulation of the Hippo pathway is a driver for cancer progression and treatment resistance. In the context of gastric cancer, YAP1 is a biomarker for poor patient prognosis. Although genomic tumor profiling provides information of Hippo pathway activation, the present study demonstrates that inhibition of Yap1 activity has anti-tumor effects in gastric tumors driven by oncogenic mutations and inflammatory cytokines. We show that Yap1 is a key regulator of cell metabolism, proliferation, and immune responses in normal and neoplastic gastric epithelium. We propose that the Hippo pathway is targetable across gastric cancer subtypes and its therapeutic benefits are likely to be mediated by both cancer cell-intrinsic and -extrinsic mechanisms.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias Gástricas Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article
Texto completo
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XML
PubMed Links
Buscar no Google

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias Gástricas Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article