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AAVC-I promotes apoptosis of human oral squamous cell carcinoma through the mitochondrial pathway.
Int J Clin Exp Pathol. 2019; 12(10):3968-3974.IJ

Abstract

This study aimed to explore the role and possible mechanism of component I from agkistrodon acutus venom (AAVC-I) in promoting the apoptosis of oral squamous cell carcinoma (OSCC). HN4 cells (a human OSCC cell line) were randomly divided into four experimental groups: low AAVC-I (2.5 μg/mL) group, medium AAVC-I (5 μg/mL) group and high AAVC-I (10 μg/mL) group, as well as control group (AAVC-I, 0 μg/mL). AVVC-I was dissolved in RPMI-1640 medium and added to the culture wells at different concentrations when tumor cells had reached the logarithmic growth phase. After 24 hours, cells were harvested and the inhibitory rate of cell proliferation and the mitochondrial membrane depolarization were measured. Western blotting was used to detect the expression levels of cytochrome c, Bcl-2 associated X protein (Bax), and caspase-3 in the cellular cytoplasm either containing mitochondria or following the removal of mitochondria. Cellular apoptosis was detected by flow cytometry. Compared to the control group, AAVC-I treatment not only inhibited NH4 growth, but also upgraded the expression of caspase-3 in NH4 cells. Meanwhile, it was observed that Bax translocation to mitochondria and cytochrome c release into the cytosol increased in AAVC-I treatment. This indicated that AAVC-I could disrupt mitochondrial membrane depolarization and result in cellular apoptosis, and the apoptosis rate of NH4 increased with the concentration of AAVC-I. The data suggested that AAVC-I promotes the apoptosis of HN4 cells through the mitochondrial pathway in a dose-dependent manner, which provides experimental data and new ideas for future research and clinical treatment options for OSCC.

Authors+Show Affiliations

School of Stomatology, Wannan Medical College 22 West Wenchang Road, Wuhu 241002, Anhui Province, China.Department of Pathophysiology, Wannan Medical College 22 West Wenchang Road, Wuhu 241002, Anhui Province, China.Department of Pathophysiology, Wannan Medical College 22 West Wenchang Road, Wuhu 241002, Anhui Province, China.School of Stomatology, Wannan Medical College 22 West Wenchang Road, Wuhu 241002, Anhui Province, China.School of Stomatology, Wannan Medical College 22 West Wenchang Road, Wuhu 241002, Anhui Province, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31933792

Citation

Chai, Lin, et al. "AAVC-I Promotes Apoptosis of Human Oral Squamous Cell Carcinoma Through the Mitochondrial Pathway." International Journal of Clinical and Experimental Pathology, vol. 12, no. 10, 2019, pp. 3968-3974.
Chai L, Huang T, Wang Z, et al. AAVC-I promotes apoptosis of human oral squamous cell carcinoma through the mitochondrial pathway. Int J Clin Exp Pathol. 2019;12(10):3968-3974.
Chai, L., Huang, T., Wang, Z., Xu, R., & Deng, C. (2019). AAVC-I promotes apoptosis of human oral squamous cell carcinoma through the mitochondrial pathway. International Journal of Clinical and Experimental Pathology, 12(10), 3968-3974.
Chai L, et al. AAVC-I Promotes Apoptosis of Human Oral Squamous Cell Carcinoma Through the Mitochondrial Pathway. Int J Clin Exp Pathol. 2019;12(10):3968-3974. PubMed PMID: 31933792.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - AAVC-I promotes apoptosis of human oral squamous cell carcinoma through the mitochondrial pathway. AU - Chai,Lin, AU - Huang,Tingting, AU - Wang,Zhenjie, AU - Xu,Ran, AU - Deng,Chao, Y1 - 2019/10/01/ PY - 2019/09/05/received PY - 2019/09/24/accepted PY - 2020/1/15/entrez PY - 2020/1/15/pubmed PY - 2020/1/15/medline KW - Component I from agkistrodon acutus venom KW - apoptosis KW - mitochondria KW - oral squamous cell carcinoma SP - 3968 EP - 3974 JF - International journal of clinical and experimental pathology JO - Int J Clin Exp Pathol VL - 12 IS - 10 N2 - This study aimed to explore the role and possible mechanism of component I from agkistrodon acutus venom (AAVC-I) in promoting the apoptosis of oral squamous cell carcinoma (OSCC). HN4 cells (a human OSCC cell line) were randomly divided into four experimental groups: low AAVC-I (2.5 μg/mL) group, medium AAVC-I (5 μg/mL) group and high AAVC-I (10 μg/mL) group, as well as control group (AAVC-I, 0 μg/mL). AVVC-I was dissolved in RPMI-1640 medium and added to the culture wells at different concentrations when tumor cells had reached the logarithmic growth phase. After 24 hours, cells were harvested and the inhibitory rate of cell proliferation and the mitochondrial membrane depolarization were measured. Western blotting was used to detect the expression levels of cytochrome c, Bcl-2 associated X protein (Bax), and caspase-3 in the cellular cytoplasm either containing mitochondria or following the removal of mitochondria. Cellular apoptosis was detected by flow cytometry. Compared to the control group, AAVC-I treatment not only inhibited NH4 growth, but also upgraded the expression of caspase-3 in NH4 cells. Meanwhile, it was observed that Bax translocation to mitochondria and cytochrome c release into the cytosol increased in AAVC-I treatment. This indicated that AAVC-I could disrupt mitochondrial membrane depolarization and result in cellular apoptosis, and the apoptosis rate of NH4 increased with the concentration of AAVC-I. The data suggested that AAVC-I promotes the apoptosis of HN4 cells through the mitochondrial pathway in a dose-dependent manner, which provides experimental data and new ideas for future research and clinical treatment options for OSCC. SN - 1936-2625 UR - https://www.unboundmedicine.com/medline/citation/31933792/AAVC-I_promotes_apoptosis_of_human_oral_squamous_cell_carcinoma_through_the_mitochondrial_pathway L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/31933792/ DB - PRIME DP - Unbound Medicine ER -
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