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Cell Death Discov. 2017 Apr 24;3:17014. doi: 10.1038/cddiscovery.2017.14. eCollection 2017.

Inducement of apoptosis by cucurbitacin E, a tetracyclic triterpenes, through death receptor 5 in human cervical cancer cell lines.

Author information

1
Department of Obstetrics and Gynecology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
2
Department of Gynecology and Obstetrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
3
Department of Obstetrics & Gynecology, E-Da Hospital, E-Da Hospital/I-Shou University, Kaohsiung, Taiwan.
4
Graduate Institute of Medical Science, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan.
5
Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
6
Department of Obstetrics and Gynecology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine Kaohsiung, Kaohsiung, Taiwan.
7
Bachelor Degree Program of Medical Sciences Industry, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan.

Abstract

Cervical cancer is the most common malignancy in women, for which conization or hysterectomy are the main therapy. Curcubitacin E (Cu E) is a natural compound-based drug which from the Guadi (climbing stem of Cucumic melo L). Previously shown to be an anti-tumor as well as a potent chemopreventive agent against several types of tumors. The present study, investigated anti-proliferation and apoptosis induced by Cu E in cervical cancer cell lines (HeLa and Ca Ski). The results indicate that the cytotoxicity is associated with accumulation in apoptosis but not necrosis. Cu E produced apoptosis as well as the up-regulation the expression of death receptor 5 (DR5). In addition, the DR5 gene activation in apoptosis, both effects increased proportionally with the dose of Cu E; however, mitosis delay was also dependant on the amount of Cu E treatment in the cancer cells. These results indicate that Cu E may delay cancer cell growth by apoptosis via upregulation of DR5 gene expression.

Conflict of interest statement

The authors declare no conflict of interest.

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