期刊
MOLECULAR MEDICINE REPORTS
卷 13, 期 3, 页码 2791-2800出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.4845
关键词
kaempferol; apoptosis; endoplasmic reticulum stress; C; EBP homologous protein; hepatocellular carcinoma cell
资金
- China National Key Project of the Twelfth Five-year Plan [2012ZX10002005-003-003]
- National Natural Science Foundation of China [81270532]
- Beijing Excellent Talents Training Fund [2011D003034000022]
- Technology Foundation for Selected Overseas Chinese Scholar, Ministry of Personnel of Beijing
- Applied Research for the Clinical Characteristics of Capital grant [Z1211070010112167]
- Special Funded Projects for 'Excellent Academic Staff' of Beijing Health Systems grant [2013-3-175, 2011-3-082]
- Cooperation Research Project of CMU and Clinical [13JL33]
Kaempferol is a flavonoid compound that has gained importance due to its antitumor properties; however, the underlying mechanisms remain to be fully understood. The present study aimed to investigate the molecular mechanisms of the antitumor function of kaempferol in HepG2 hepatocellular carcinoma cells. Kaempferol was determined to reduce cell viability, increase lactate dehydrogenase activity and induce apoptosis in a concentration- and time-dependent manner in HepG2 cells. Additionally, kaempferol-induced apoptosis possibly acts via the endoplasmic reticulum (ER) stress pathway, due to the significant increase in the protein expression levels of glucose-regulated protein 78, glucose-regulated protein 94, protein kinase R-like ER kinase, inositol-requiring enzyme 1, partial activating transcription factor 6 cleavage, caspase-4, C/EBP homologous protein (CHOP) and cleaved caspase-3. The pro-apoptotic activity of kaempferol was determined to be due to induction of the ER stress-CHOP pathway, as: i) ER stress was blocked by 4-phenyl butyric acid (4-PBA) pretreatment and knockdown of CHOP with small interfering RNA, which resulted in alleviation of kaempferol-induced HepG2 cell apoptosis; and ii) transfection with plasmid overexpressing CHOP reversed the protective effect of 4-PBA in kaempferol-induced HepG2 cells and increased the apoptotic rate. Thus, kaempferol promoted HepG2 cell apoptosis via induction of the ER stress-CHOP signaling pathway. These observations indicate that kaempferol may be used as a potential chemopreventive treatment strategy for patients with hepatocellular carcinoma.
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