AI Article Synopsis

  • Metabolic changes in the tumour microenvironment help cancer cells survive and resist treatments, driven by inflammation from adipose (fat) tissue.
  • STAT3 is identified as a key player in these metabolic changes, influencing cancer cell behavior by responding to signals from adipose tissue and other inflammatory factors.
  • The review highlights how the interplay between STAT3's functions in gene regulation and mitochondrial activity supports cancer cell survival and growth, particularly in the context of breast cancer related to fat tissue.

Article Abstract

Metabolic remodelling of the tumour microenvironment is a major mechanism by which cancer cells survive and resist treatment. The pro-oncogenic inflammatory cascade released by adipose tissue promotes oncogenic transformation, proliferation, angiogenesis, metastasis and evasion of apoptosis. STAT3 has emerged as an important mediator of metabolic remodelling. As a downstream effector of adipocytokines and cytokines, its canonical and non-canonical activities affect mitochondrial functioning and cancer metabolism. In this review, we examine the central role played by the crosstalk between the transcriptional and mitochondrial roles of STAT3 to promote survival and further oncogenesis within the tumour microenvironment with a particular focus on adipose-breast cancer interactions.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226520PMC
http://dx.doi.org/10.3390/cells9041043DOI Listing

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