Tomentosin inhibits cell proliferation and induces apoptosis in MOLT‐4 leukemia cancer cells through the inhibition of mTOR/PI3K/Akt signaling pathway.

Autor: Yang, Linlin, Xie, Jin, Almoallim, Hesham S., Alharbi, Sulaiman A., Chen, Yanli
Předmět:
Zdroj: Journal of Biochemical & Molecular Toxicology; Apr2021, Vol. 35 Issue 4, p1-8, 8p
Abstrakt: Leukemia is amongst the cancers accountable for substantial mortality around the world. Tomentosin is a bioactive compound with a pharmacological significance, and its anticancer property against human leukemia MOLT‐4 cell line has never been reported. Hence, the objective of this study was to explore the anticancer activity of tomentosin in MOLT‐4 human leukemia cells. In the current investigation, the cytotoxic effects of tomentosin ensuing potent toxicity (IC50: 10 µM) in MOLT‐4 cells after incubation at 24 h have been presented. Furthermore, tomentosin triggered intracellular reactive oxygen species production and showed the induction of intrinsic/mitochondrial pathways in treated MOLT‐4 cells, revealing a significant cytotoxicity activity. Also, fluorescent microscopic studies using acridine orange/ethidium bromide and propidium iodide staining confirmed the occurrence of apoptosis in tomentosin‐treated MOLT‐4 cells. Quantitative reverse transcription polymerase chain reaction presented a negative regulation of cyclin D1 and BcL‐2 expression and a positive regulated BAX and caspase‐3 messenger RNA expression in tomentosin‐treated MOLT‐4 cells. Tomentosin further inhibited the inflammatory transcription factors such as nuclear factor κB (NF‐κB), tumor necrosis factor α, interleukin 1β (IL‐1β), and IL‐6. Additionally, inhibition of the m‐TOR/PI3K/AKT protein expression by tomentosin in MOLT‐4 cells was confirmed. Overall, these findings lead to a conclusion that tomentosin induces apoptosis in MOLT‐4 cells through caspase‐facilitated proapoptotic pathway, and inhibition of the NF‐κB‐stimulated Bcl‐2 facilitated the antiapoptotic pathway. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index