期刊
ONCOTARGET
卷 8, 期 47, 页码 82207-82216出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.19200
关键词
kaempferol; hepatocellular carcinoma cell; endoplasmic reticulum stress; C/EBP homologous protein; autophagy
资金
- National Natural Science Foundation of China [81270532]
- Natural Science Foundation of Beijing [7162085]
- Beijing Municipal Science & Technology Commission [Z161100000516113]
- High-level Technical Personnel Training Plan of the Beijing Health System [2013-3-075]
- National Science and Technology Major Project [2016ZX10002008-04, 2016ZX10004906-014]
- Project of Construction of Innovative Teams and Teacher Career Development for Universities and Colleges Under Beijing Municipality [IDHT20150502]
- Science and Technology New Star Program of Beijing Fengtai District
Kaempferol is a flavonoid compound that has gained widespread attention due to its antitumor functions. However, the underlying mechanisms are still not clear. The present study investigated the effect of kaempferol on hepatocellular carcinoma and its underlying mechanisms. Kaempferol induced autophagy in a concentration-and time-dependent manner in HepG2 or Huh7 cells, which was evidenced by the significant increase of autophagy-related genes. Inhibition of autophagy pathway, through 3-methyladenine or Atg7 siRNA, strongly diminished kaempferol-induced apoptosis. We further hypothesized that kaempferol can induce autophagy via endoplasmic reticulum (ER) stress pathway. Indeed, blocking ER stress by 4-phenyl butyric acid (4-PBA) or knockdown of CCAAT/enhancer-binding protein homologous protein (CHOP) with siRNA alleviated kaempferol-induced HepG2 or Huh7 cells autophagy; while transfection with plasmid overexpressing CHOP reversed the effect of 4-PBA on kaempferol-induced autophagy. Our results demonstrated that kaempferol induced hepatocarcinoma cell death via ER stress and CHOP-autophagy signaling pathway; kaempferol may be used as a potential chemopreventive agent for patients with hepatocellular carcinoma.
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