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Induction of apoptosis by 7-piperazinethylchrysin in HCT-116 human colon cancer cells.
Oncol Rep. 2012 Nov; 28(5):1719-26.OR

Abstract

The antitumor activity of 7-piperazinethylchrysin (7-PEC) was investigated in HCT-116 human colon cancer cells. MTT assay revealed that the IC50 of 7-PEC in HCT-116 cells was 1.5 µM after 72 h of treatment, much lower than that of chrysin (>100 µM). The data showed that 7-PEC was able to inhibit the growth of HCT-116 cells in a concentration- and time-dependent manner. Topical morphological changes of apoptotic body formation after 7-PEC treatment were observed by Hoechst 33258 staining. 7-PEC reduced mitochondrial membrane potential (∆Ψm) of cells in a concentration-dependent manner and increased the production of intracellular reactive oxygen species (ROS). After treatment with 7-PEC, a significant increase of Bax protein expression and decrease of Bcl-2 protein expression were observed at the same time. These events paralleled with activation of p53, caspase-3 and -9 and the release of cytochrome c (cyt‑c), as well as poly(ADP-ribose) polymerase-1 (PARP1) cleavage and downregulation of p-Akt. However, the apoptosis induced by 7-PEC was blocked by Ac-DEVD-CHO, a caspase-3 inhibitor. These results demonstrate that 7-PEC-induced mitochondrial dysfunction in HCT-116 human colon cancer cells triggers events responsible for caspase-dependent apoptosis pathways, and the elevated ratio of Bax/Bcl-2 is likely involved in this effect.

Authors+Show Affiliations

School of Pharmaceutical Engineering and Life Science, Changzhou University, Changzhou, Jiangsu 213164, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22948973

Citation

Ren, Jie, et al. "Induction of Apoptosis By 7-piperazinethylchrysin in HCT-116 Human Colon Cancer Cells." Oncology Reports, vol. 28, no. 5, 2012, pp. 1719-26.
Ren J, Cheng H, Xin WQ, et al. Induction of apoptosis by 7-piperazinethylchrysin in HCT-116 human colon cancer cells. Oncol Rep. 2012;28(5):1719-26.
Ren, J., Cheng, H., Xin, W. Q., Chen, X., & Hu, K. (2012). Induction of apoptosis by 7-piperazinethylchrysin in HCT-116 human colon cancer cells. Oncology Reports, 28(5), 1719-26. https://doi.org/10.3892/or.2012.2016
Ren J, et al. Induction of Apoptosis By 7-piperazinethylchrysin in HCT-116 Human Colon Cancer Cells. Oncol Rep. 2012;28(5):1719-26. PubMed PMID: 22948973.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Induction of apoptosis by 7-piperazinethylchrysin in HCT-116 human colon cancer cells. AU - Ren,Jie, AU - Cheng,Hong, AU - Xin,Wen Qun, AU - Chen,Xin, AU - Hu,Kun, Y1 - 2012/09/04/ PY - 2012/07/09/received PY - 2012/08/13/accepted PY - 2012/9/6/entrez PY - 2012/9/6/pubmed PY - 2013/3/15/medline SP - 1719 EP - 26 JF - Oncology reports JO - Oncol Rep VL - 28 IS - 5 N2 - The antitumor activity of 7-piperazinethylchrysin (7-PEC) was investigated in HCT-116 human colon cancer cells. MTT assay revealed that the IC50 of 7-PEC in HCT-116 cells was 1.5 µM after 72 h of treatment, much lower than that of chrysin (>100 µM). The data showed that 7-PEC was able to inhibit the growth of HCT-116 cells in a concentration- and time-dependent manner. Topical morphological changes of apoptotic body formation after 7-PEC treatment were observed by Hoechst 33258 staining. 7-PEC reduced mitochondrial membrane potential (∆Ψm) of cells in a concentration-dependent manner and increased the production of intracellular reactive oxygen species (ROS). After treatment with 7-PEC, a significant increase of Bax protein expression and decrease of Bcl-2 protein expression were observed at the same time. These events paralleled with activation of p53, caspase-3 and -9 and the release of cytochrome c (cyt‑c), as well as poly(ADP-ribose) polymerase-1 (PARP1) cleavage and downregulation of p-Akt. However, the apoptosis induced by 7-PEC was blocked by Ac-DEVD-CHO, a caspase-3 inhibitor. These results demonstrate that 7-PEC-induced mitochondrial dysfunction in HCT-116 human colon cancer cells triggers events responsible for caspase-dependent apoptosis pathways, and the elevated ratio of Bax/Bcl-2 is likely involved in this effect. SN - 1791-2431 UR - https://www.unboundmedicine.com/medline/citation/22948973/Induction_of_apoptosis_by_7_piperazinethylchrysin_in_HCT_116_human_colon_cancer_cells_ L2 - http://www.spandidos-publications.com/or/28/5/1719 DB - PRIME DP - Unbound Medicine ER -