1. Active fraction of clove induces apoptosis via PI3K/Akt/mTOR-mediated autophagy in human colorectal cancer HCT-116 cells.
- Author
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Liu M, Zhao G, Zhang D, An W, Lai H, Li X, Cao S, and Lin X
- Subjects
- Adenine analogs & derivatives, Adenine pharmacology, Antineoplastic Agents, Phytogenic therapeutic use, Autophagy drug effects, Cell Proliferation drug effects, Cell Survival drug effects, Colorectal Neoplasms pathology, Drug Screening Assays, Antitumor, HCT116 Cells, Humans, Macrolides pharmacology, Phosphatidylinositol 3-Kinases metabolism, Plant Extracts therapeutic use, Proto-Oncogene Proteins c-akt metabolism, Signal Transduction drug effects, Sirolimus pharmacology, TOR Serine-Threonine Kinases metabolism, Antineoplastic Agents, Phytogenic pharmacology, Apoptosis drug effects, Colorectal Neoplasms drug therapy, Plant Extracts pharmacology, Syzygium chemistry
- Abstract
Previous studies by our group have demonstrated that extract of clove exhibits potent anticancer effects in vitro and in vivo. In the present study, the effect of an extracted and isolated active fraction of clove (AFC) on induction of cellular apoptosis in human colorectal cancer HCT-116 cells was investigated by morphological observation, flow cytometry, and western blotting analysis. The results revealed that AFC induced apoptosis of HCT-116 cells. AFC also induced autophagy, demonstrated by increased punctuate microtubule-associated protein 1A/1B-light chain 3 (LC3) staining, and LC3-II and Beclin-1 protein expression levels. Furthermore, the autophagy inhibitors 3-MA and baflomycin A1 potentiated the pro-apoptotic activity of AFC in HCT-116 cells. AFC also inhibited the phosphorylation of the phosphoinositide 3-kinase/Akt/mechanistic target of rapamycin signaling pathway. The present study may improve the existing understanding of the anticancer mechanisms of clove and provide a scientific rationale for AFC to be further developed as a promising novel anticancer agent for the treatment of colorectal cancer.
- Published
- 2018
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