Genipin increases oxaliplatin-induced cell death through autophagy in gastric cancer

Oxaliplatin is used for treatment in combination with many drugs. However, the survival rate is still low due to side effects and drug resistance. Therefore, the combination with natural products was required for increasing efficacy and reducing side effects. Genipin, a natural product derived from...

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Bibliographic Details
Published in:Journal of Cancer 2020, Vol.11 (2), p.460-467
Main Authors: Kim, Bo Ram, Jeong, Yoon A, Kim, Dae Young, Kim, Jung Lim, Jeong, Soyeon, Na, Yoo Jin, Yun, Hye Kyeong, Park, Seong Hye, Jo, Min Jee, Ashktorab, Hassan, Smoot, Duane T, Lee, Dae-Hee, Oh, Sang Cheul
Format: Article
Language:English
Subjects:
Antibodies
Apoptosis
Autophagy
Cancer therapies
Cell culture
Cell death
Flow cytometry
Gastric cancer
Laboratories
Membranes
Microscopy
Morphology
Natural products
Proteins
Reagents
Research Paper
Statistical analysis
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Summary:Oxaliplatin is used for treatment in combination with many drugs. However, the survival rate is still low due to side effects and drug resistance. Therefore, the combination with natural products was required for increasing efficacy and reducing side effects. Genipin, a natural product derived from the , associated with anti-angiogenic, anti-proliferative, hypertension, inflammatory, and the Hedgehog pathway. It is not known that genipin increases the therapeutic effect of oxaliplatin in gastric cancer. In this study, we found that genipin sensitizes oxaliplatin-induced apoptosis for the first time using colony forming assay, FACS analysis, and western blotting in gastric cancer. Additionally, genipin induced p53 expression in AGS, MKN45, and MKN28 cells. Also, genipin induced autophagy and LC3 expression. Knockdown of LC3 decreased cell death enhanced by the combination of oxaliplatin and genipin. In summary, we showed that genipin increases the oxaliplatin-induced cell death via p53-DRAM autophagy. Based on this, we suggest that genipin is a sensitizer of oxaliplatin.
ISSN:1837-9664
1837-9664
DOI:10.7150/jca.34773