Mitogen-Activated Protein Kinase (MAPK) and Obesity-Related Cancer

Fionán Donohoe1, Michael Wilkinson1, Eva Baxter2

  • 1Ireland East Hospital Gynaeoncology Group, UCD School of Medicine, Mater Misericordiae University, D07R2WY Dublin 7, Ireland.

Insights

Obesity increases cancer risk through complex molecular pathways. This review explores how mitogen-activated protein kinase (MAPK) signaling contributes to obesity-related cancers, focusing on p38 and JNK pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Public Health

Background:

  • Obesity is a global health issue linked to increased cancer incidence.
  • The molecular mechanisms connecting obesity and cancer remain incompletely understood.
  • Mitogen-activated protein kinase (MAPK) signaling pathways are implicated in cellular processes relevant to cancer development.

Purpose of the Study:

  • To review the role of MAPK signaling in obesity-related cancers.
  • To elucidate the molecular links between MAPK pathways (p38, JNK) and cancer development in obesity.
  • To identify potential areas for future research in this field.

Main Methods:

  • Literature review focusing on MAPK signaling pathways (p38, JNK, ERK).
  • Analysis of MAPK involvement in obesity-related immune dysfunction.
  • Examination of MAPK effects on endoplasmic reticulum stress and aromatase activation.

Main Results:

  • MAPK signaling, particularly p38 and JNK, plays a role in obesity-related immune paralysis.
  • MAPK pathways influence endoplasmic reticulum stress responses relevant to cancer.
  • MAPK activation is linked to aromatase activity, a factor in hormone-sensitive cancers.

Conclusions:

  • MAPK signaling is a key mediator linking obesity to increased cancer risk.
  • Further research into p38 and JNK pathways could reveal therapeutic targets for obesity-related cancers.
  • Specific cancers like endometrioid endometrial cancer and hepatocellular carcinoma (associated with NAFLD/NASH) offer promising avenues for investigation.

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