Abstract

Autophagy (macroautophagy) is an evolutionarily conserved lysosomal degradation process, in which a cell degrades long-lived proteins and damaged organelles. Recently, accumulating evidence has revealed the core molecular machinery of autophagy in carcinogenesis; however, the intricate relationship between autophagy and cancer continue to remain an enigma. Why does autophagy have either pro-survival (oncogenic) or pro-death (tumor suppressive) role at different cancer stages, including cancer stem cell, initiation and progression, invasion and metastasis, as well as dormancy? How does autophagy modulate a series of oncogenic and/or tumor suppressive pathways, implicated in microRNA (miRNA) involvement? Whether would targeting the oncogenic and tumor suppressive autophagic network be a novel strategy for drug discovery? To address these problems, we focus on summarizing the dynamic oncogenic and tumor suppressive roles of autophagy and their relevant small-molecule drugs, which would provide a new clue to elucidate the oncosuppressive (survival or death) autophagic network as a potential therapeutic target.

Highlights

  • Autophagy, an evolutionarily conserved lysosomal degradation process, is well-suited to have the role of the Roman God Janus in sealing the fate of cancer cells: survival or death

  • Why does autophagy have either pro-survival or pro-death role at different cancer stages, including cancer stem cell, initiation and progression, invasion and metastasis, as well as dormancy? How does autophagy modulate a series of oncogenic and/or tumor suppressive pathways, implicated in microRNA involvement? Whether would targeting the oncogenic and tumor suppressive autophagic network be a novel strategy for drug discovery? To address these problems, we focus on summarizing the dynamic oncogenic and tumor suppressive roles of autophagy and their relevant small-molecule drugs, which would provide a new clue to elucidate the oncosuppressive autophagic network as a potential therapeutic target

  • As an evolutionary conserved lysosomal degradation process, autophagy may play the Janus role by regulating some oncogenes (e.g., PI3KCI, Akt, mTORC1, Ras, Raf and BCRABL) or other tumor suppressors (e.g., Beclin-1, p53, FoxO1 and BNIP-3), which is implicated in autophagic relevant pathways to jointly seal the fate of cancer cell

Read more

Summary

Open Questions

Why does autophagy have either pro-survival (oncogenic) or pro-death (tumor suppressive) role at specific cancer stage, including CSC, initiation and progression, invasion and metastasis and dormancy?. The complete autophagic flow is a highly regulated process that can generally be divided into the following five stages: induction, vesicle nucleation, vesicle elongation and completion, docking and fusion, and degradation and recycling.[3] Induction of autophagy is initiated by the ULK complex, which. These paradoxical studies are often confusing, depending on different cell types, autophagy seems to have either an oncogenic or tumor suppressive role for the regulation of core pathways, thereby sealing the distinctive. This review summarizes the Janus role of autophagy at different cancer cell stages, oncogenic and tumor suppressive autophagic pathways involved in miRNAs, as well as relevant autophagy-modulated drugs in cancer therapy

Autophagy and Cancer Cell
Oncosuppressive Autophagic Pathways in Cancer
Oncogenic and Tumor Suppressive miRNAs in Autophagy
Autophagic Network as a Cancer Therapeutic Target
Conclusions
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.