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PPAR α  (peroxisome-proliferator-activated receptor  α ) plays a critical role in regulation of inflammation and cancer, while the regulatory mechanism of PPAR α  on cancer cell autophagy is still unclear. Here we found that PPAR α  enhanced autophagy in HEK293T, SW480, and Hela cell lines, which was independent of PPAR α  transcription activity. PPAR α  induced antiapoptotic Bcl2 protein degradation resulting in release of the Beclin-1/VPS34 complex. Consistently, silenced PPAR α  reversed this event. PPAR α -induced autophagy significantly inhibited tumor growth and enhanced SW480 cancer cell sensitivity to chemotherapy drugs. Moreover, PPAR α  agonist increased SW480 cancer cell chemotherapy sensitivity. These findings revealed a novel mechanism of PPAR α /Bcl2/autophagy pathway suppressed tumor progression and enhanced chemotherapy sensitivity, which is a potential drug target for cancer treatment.

journal of oncology

PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math> Enhances Cancer Cell Chemotherapy Sensitivity by Autophagy Induction

PPARα Enhances Cancer Cell Chemotherapy Sensitivity by Autophagy Induction