Abstract Title:

Bufalin induced apoptosis in SCC‑4 human tongue cancer cells by decreasing Bcl‑2 and increasing Bax expression via the mitochondria‑dependent pathway.

Abstract Source:

Mol Med Rep. 2017 Dec ;16(6):7959-7966. Epub 2017 Sep 28. PMID: 28983595

Abstract Author(s):

Han-Yu Chou, Fu-Shin Chueh, Yi-Shih Ma, Rick Sai-Chuen Wu, Ching-Lung Liao, Yung-Lin Chu, Ming-Jen Fan, Wen-Wen Huang, Jing-Gung Chung

Article Affiliation:

Han-Yu Chou


The aim of the present study was to investigate the cytotoxic effects of bufalin on SCC‑4 human tongue cancer cells. Cell morphological changes and viability were examined using phase contrast microscopy and flow cytometry, respectively. The results indicated that bufalin induced morphological changes and reduced total viable cells. Apoptotic cell death was analyzed by DAPI stainingand DNA gel electrophoresis; the results revealed that bufalin induced cell apoptosis. Levels of reactive oxygen species (ROS), Ca2+, nitric oxide (NO) and mitochondrial membrane potential (ΔΨm) were measured by flow cytometry, and bufalin was observed to increase Ca2+ and NO production, decreasethe ΔΨm and reduce ROS production in SCC‑4 cells. In addition, western blotting was performed to detect apoptosis‑associated protein expression. The results demonstrated that bufalin reduced the expression of the anti‑apoptotic protein B‑cell lymphoma 2 (Bcl‑2) and increased the expression of the pro‑apoptotic protein, Bcl‑2‑associated X protein. However, bufalin treatment also increased the expression of other apoptosis‑associated proteins such as apoptosis‑inducing factor and endonuclease G in SCC‑4 cells. Based on these findings, bufalin may induce apoptotic cell death via mitochondria‑dependent pathways in human tongue cancer SCC‑4 cells.

Study Type : In Vitro Study

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