Autophagy and EMT in cancer and metastasis: Who controls whom?

Area of Science:

• Oncology
• Cell Biology
• Molecular Biology

Background:

• Metastasis involves complex cellular events like Epithelial-Mesenchymal Transition (EMT), angiogenesis, and immune evasion.
• Autophagy, a cellular degradation process, is increasingly recognized for its significant and often contradictory roles in cancer.
• The intricate relationship between autophagy and EMT in cancer metastasis remains an active area of research.

Purpose of the Study:

• To elucidate the multifaceted relationship between autophagy and Epithelial-Mesenchymal Transition (EMT) in the context of cancer metastasis.
• To review the dual role of autophagy in promoting and suppressing metastatic processes.
• To discuss the potential of targeting EMT through autophagy modulation as a therapeutic strategy.

Main Methods:

• Literature review and synthesis of existing research on autophagy, EMT, and cancer metastasis.
• Analysis of evidence detailing the mechanisms by which autophagy influences EMT markers and processes.
• Exploration of studies investigating the oncosuppressive and oncomodulatory functions of autophagy in metastasis.

Main Results:

• Autophagy is essential for cancer cell survival during EMT, migration, and dissemination.
• Autophagy can orchestrate EMT markers, influencing cancer cell plasticity.
• Conversely, autophagy demonstrates oncosuppressive functions by impeding early metastatic events.

Conclusions:

• Autophagy and EMT exhibit reciprocal roles with significant consequences for cancer metastasis.
• Targeting EMT via modulation of autophagy presents a promising therapeutic avenue.
• Further research into this complex interplay is crucial for developing effective anti-metastatic treatments.