Key result
Adipokines secreted by adipose tissue, such as leptin and adiponectin, mediate the crosstalk between obesity and cancer development through multiple signaling pathways.
This review highlights the mechanisms by which adipokines secreted by adipose tissue link obesity to cancer development and progression.
Adipokine dysregulation may guide mechanistic research on obesity-cancer links; leaves open clinical relevance of leptin pathway targeting.
Adipose tissue is a complex organ that is increasingly being recognised as the largest endocrine organ in the body. Adipocytes among multiple cell types of adipose tissue can secrete a variety of adipokines, which are involved in signalling pathways and these can be changed by obesity and cancer. There are proposed mechanisms to link obesity/adiposity to cancer development including adipocytokine dysregulation. Among these adipokines, leptin acts through multiple pathways including the STAT3, MAPK, and PI3K pathways involved in cell growth. Adiponectin has the opposite action from leptin in tumour growth partly because of increased apoptotic responses of p53 and Bax. Visfatin increases cancer cell proliferation through ERK1/2, PI3K/AKT, and p38 which are stimulated by proinflammatory cytokines. Omentin through the PI3K/Akt-Nos pathway is involved in cancer-tumour development. Apelin might be involved through angiogenesis in tumour progressions. PAI-1 via its anti-fibrinolytic activity on cell adhesion and uPA/uPAR activity influence cancer cell growth.
No takes yet. Share an insight, caveat, or question.
Tahergorabi et al. (2021) conducted a review in Obesity and cancer. Adipokines was evaluated. Adipokines secreted by adipose tissue, such as leptin and adiponectin, mediate the crosstalk between obesity and cancer development through multiple signaling pathways.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: