JNK in Tumor Microenvironment: Present Findings and Challenges in Clinical Translation

Area of Science:

• Cellular signaling pathways
• Cancer biology
• Immunology

Background:

• c-Jun N-terminal kinases (JNK) are mitogen-activated protein kinases (MAPKs) activated by stress and inflammatory cytokines.
• JNK signaling regulates critical cellular processes including proliferation, differentiation, survival, and apoptosis.
• JNK exhibits context-dependent roles in cancer, acting as both a tumor promoter and suppressor.

Purpose of the Study:

• To review the multifaceted roles of the JNK pathway within the tumor microenvironment (TME).
• To elucidate JNK-mediated processes in TME, including responses to hypoxia, oxidative stress, and inflammation.
• To highlight JNK's involvement in immune responses, angiogenesis, and cellular regulation within the TME.

Main Methods:

• Literature review of existing studies on JNK signaling in cancer and TME.
• Synthesis of current knowledge on JNK's downstream targets and mediating roles.
• Identification of research gaps and future directions for therapeutic translation.

Main Results:

• JNK signaling is intricately involved in various tumorigenesis pathways.
• The TME, characterized by stress and inflammation, presents complex scenarios for JNK pathway modulation.
• JNK influences diverse cellular components and processes within the TME, impacting tumor development.

Conclusions:

• Understanding JNK's complex roles in the TME is crucial for cancer research.
• Targeting the JNK pathway holds potential for therapeutic strategies in oncology.
• Further research is needed to translate preclinical findings into clinical benefits for cancer patients.