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PPARα Enhances Cancer Cell Chemotherapy Sensitivity by Autophagy Induction
Joint Authors
Hou, Yongzhong
Jin, Jianhua
You, Mengli
Gao, Jiaming
Source
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-8, 8 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-11-04
Country of Publication
Egypt
No. of Pages
8
Main Subjects
Abstract EN
PPARα (peroxisome-proliferator-activated receptor α) plays a critical role in regulation of inflammation and cancer, while the regulatory mechanism of PPARα on cancer cell autophagy is still unclear.
Here we found that PPARα enhanced autophagy in HEK293T, SW480, and Hela cell lines, which was independent of PPARα transcription activity.
PPARα induced antiapoptotic Bcl2 protein degradation resulting in release of the Beclin-1/VPS34 complex.
Consistently, silenced PPARα reversed this event.
PPARα-induced autophagy significantly inhibited tumor growth and enhanced SW480 cancer cell sensitivity to chemotherapy drugs.
Moreover, PPARα agonist increased SW480 cancer cell chemotherapy sensitivity.
These findings revealed a novel mechanism of PPARα/Bcl2/autophagy pathway suppressed tumor progression and enhanced chemotherapy sensitivity, which is a potential drug target for cancer treatment.
American Psychological Association (APA)
You, Mengli& Gao, Jiaming& Jin, Jianhua& Hou, Yongzhong. 2018. PPARα Enhances Cancer Cell Chemotherapy Sensitivity by Autophagy Induction. Journal of Oncology،Vol. 2018, no. 2018, pp.1-8.
https://search.emarefa.net/detail/BIM-1195839
Modern Language Association (MLA)
You, Mengli…[et al.]. PPARα Enhances Cancer Cell Chemotherapy Sensitivity by Autophagy Induction. Journal of Oncology No. 2018 (2018), pp.1-8.
https://search.emarefa.net/detail/BIM-1195839
American Medical Association (AMA)
You, Mengli& Gao, Jiaming& Jin, Jianhua& Hou, Yongzhong. PPARα Enhances Cancer Cell Chemotherapy Sensitivity by Autophagy Induction. Journal of Oncology. 2018. Vol. 2018, no. 2018, pp.1-8.
https://search.emarefa.net/detail/BIM-1195839
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1195839