A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation
Oblongifolin C (OC) was identified as a potent apoptosis inducer from an herbal plant, Garcinia yunnanensis, during our previous bioassay-guided drug screening. In this study, we investigated the signaling pathways through which OC activated apoptosis in HeLa cells. We also compared the IC50 values...
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Format: | Journal Article |
Language: | English |
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2013
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Online Access: | https://hdl.handle.net/10356/102141 http://hdl.handle.net/10220/16943 |
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author | Feng, Chao Zhou, Liying Yu, Ting Xu, Gang Tian, Hong-Lei Xu, Jin-Jie Xu, Hong-Xi Luo, Kathy Qian |
author2 | School of Chemical and Biomedical Engineering |
author_facet | School of Chemical and Biomedical Engineering Feng, Chao Zhou, Liying Yu, Ting Xu, Gang Tian, Hong-Lei Xu, Jin-Jie Xu, Hong-Xi Luo, Kathy Qian |
author_sort | Feng, Chao |
collection | NTU |
description | Oblongifolin C (OC) was identified as a potent apoptosis inducer from an herbal plant, Garcinia yunnanensis, during our previous bioassay-guided drug screening. In this study, we investigated the signaling pathways through which OC activated apoptosis in HeLa cells. We also compared the IC50 values of OC with that of etoposide, paclitaxel and vinblastine in multiple cancer cell lines including HER2 and P-glycoprotein overexpressing cells. In addition, the in vivo antitumor effect of OC was studied in nude mice model. Our results showed that OC induced a caspase-dependent apoptosis by triggering a series of events in HeLa cells including Bax translocation, cytochrome c release, caspase-3 activation, chromosome fragmentation followed by caspase-8 activation, Bid cleavage and eventually cell death. Addition of a pan-caspase inhibitor or overexpression of an anti-apoptotic protein, Bcl-xL, prevented OC-induced cell death. Moreover, OC exhibited a wide anticancer spectrum in multiple cancer cell lines with comparable IC50 values, regardless of the expression levels of HER2 and P-glycoprotein. In contrast, the IC50 values of three clinical anticancer drugs, etoposide, paclitaxel and vinblastine were significantly elevated in HER2 and/or P-glycoprotein overexpressing cells. Furthermore, OC showed a similar antitumor effect but lower general toxicity than etoposide against xenografted human tumors in nude mice model. All these data suggested that OC is a promising apoptosis inducer with the potential to be developed into a clinical anticancer drug. |
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format | Journal Article |
id | ntu-10356/102141 |
institution | Nanyang Technological University |
language | English |
last_indexed | 2024-10-01T05:51:30Z |
publishDate | 2013 |
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spelling | ntu-10356/1021412020-03-07T11:35:26Z A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation Feng, Chao Zhou, Liying Yu, Ting Xu, Gang Tian, Hong-Lei Xu, Jin-Jie Xu, Hong-Xi Luo, Kathy Qian School of Chemical and Biomedical Engineering Oblongifolin C (OC) was identified as a potent apoptosis inducer from an herbal plant, Garcinia yunnanensis, during our previous bioassay-guided drug screening. In this study, we investigated the signaling pathways through which OC activated apoptosis in HeLa cells. We also compared the IC50 values of OC with that of etoposide, paclitaxel and vinblastine in multiple cancer cell lines including HER2 and P-glycoprotein overexpressing cells. In addition, the in vivo antitumor effect of OC was studied in nude mice model. Our results showed that OC induced a caspase-dependent apoptosis by triggering a series of events in HeLa cells including Bax translocation, cytochrome c release, caspase-3 activation, chromosome fragmentation followed by caspase-8 activation, Bid cleavage and eventually cell death. Addition of a pan-caspase inhibitor or overexpression of an anti-apoptotic protein, Bcl-xL, prevented OC-induced cell death. Moreover, OC exhibited a wide anticancer spectrum in multiple cancer cell lines with comparable IC50 values, regardless of the expression levels of HER2 and P-glycoprotein. In contrast, the IC50 values of three clinical anticancer drugs, etoposide, paclitaxel and vinblastine were significantly elevated in HER2 and/or P-glycoprotein overexpressing cells. Furthermore, OC showed a similar antitumor effect but lower general toxicity than etoposide against xenografted human tumors in nude mice model. All these data suggested that OC is a promising apoptosis inducer with the potential to be developed into a clinical anticancer drug. 2013-10-28T02:35:00Z 2019-12-06T20:50:16Z 2013-10-28T02:35:00Z 2019-12-06T20:50:16Z 2011 2011 Journal Article Feng, C., Zhou, L.-Y., Yu, T., Xu, G., Tian, H.-L., Xu, J.-J., Xu, H.-X., & Luo, K. Q. (2012). A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation. International Journal of Cancer, 131(6), 1445-1454. 0020-7136 https://hdl.handle.net/10356/102141 http://hdl.handle.net/10220/16943 10.1002/ijc.27365 en International journal of cancer |
spellingShingle | Feng, Chao Zhou, Liying Yu, Ting Xu, Gang Tian, Hong-Lei Xu, Jin-Jie Xu, Hong-Xi Luo, Kathy Qian A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation |
title | A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation |
title_full | A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation |
title_fullStr | A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation |
title_full_unstemmed | A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation |
title_short | A new anticancer compound, Oblongifolin C, inhibits tumor growth and promotes apoptosis in HeLa cells through bax activation |
title_sort | new anticancer compound oblongifolin c inhibits tumor growth and promotes apoptosis in hela cells through bax activation |
url | https://hdl.handle.net/10356/102141 http://hdl.handle.net/10220/16943 |
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