Int J Med Sci 2018; 15(8):832-839. doi:10.7150/ijms.23270 This issue Cite

Research Paper

Proscillaridin A induces apoptosis, inhibits STAT3 activation and augments doxorubicin toxicity in prostate cancer cells

Yangyang He1, Muhammad Khan2, Jingbo Yang3, Min Yao1, Shili Yu1, Hongwen Gao1✉

1. Department of Pathology, the Second Hospital of Jilin University, Changchun 130041, P.R. China.
2. Department of Zoology, University of the Punjab, Quaid-e-Azam Campus Lahore 54590, Pakistan.
3. Jilin Provincial Key Laboratory on Molecular and Chemical Genetics, the Second Hospital of Jilin University, Changchun 130041, P.R. China.

Citation:
He Y, Khan M, Yang J, Yao M, Yu S, Gao H. Proscillaridin A induces apoptosis, inhibits STAT3 activation and augments doxorubicin toxicity in prostate cancer cells. Int J Med Sci 2018; 15(8):832-839. doi:10.7150/ijms.23270. https://www.medsci.org/v15p0832.htm
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Abstract

Cardiac glycosides are natural compounds used for the treatment of congestive heart failure and cardiac arrhythmias. Recently, they have been reported to exhibit anticancer activity. Proscillaridin A (PSN-A), a cardiac glycoside constituent of Urginea maritima has been shown to exhibit anticancer activity. However, the cellular targets and anticancer mechanism of PSN-A in various cancers including prostate cancer remain largely unexplored. In the present study, we have shown that PSN-A inhibits proliferation and induces apoptosis in prostate cancer cells in a dose-dependent manner. Further mechanistic study have shown that anticancer activity of PSN-A in prostate cancer cells is associated with ROS generation, Bcl-2 family proteins modulation, mitochondrial membrane potential disruption and ultimately activation of caspase-3 and cleavage of PARP. Moreover, we found that PSN-A inhibits JAK2/STAT3 signaling and augments doxorubicin toxicity in prostate cancer cells. Of note, LNCaP cells were found to be more sensitive to PSN-A treatment as compared to DU145 cells. Taken together, the data provided first evidence of the anticancer activity and possible molecular mechanism of PSN-A in prostate cancer. Further study is needed to develop PSN-A into a potential lead compound for the treatment of prostate cancer.

Keywords: Cardiac glycosides, Proscillaridin A, Bcl-2, STAT3, Prostate cancer


Citation styles

APA
He, Y., Khan, M., Yang, J., Yao, M., Yu, S., Gao, H. (2018). Proscillaridin A induces apoptosis, inhibits STAT3 activation and augments doxorubicin toxicity in prostate cancer cells. International Journal of Medical Sciences, 15(8), 832-839. https://doi.org/10.7150/ijms.23270.

ACS
He, Y.; Khan, M.; Yang, J.; Yao, M.; Yu, S.; Gao, H. Proscillaridin A induces apoptosis, inhibits STAT3 activation and augments doxorubicin toxicity in prostate cancer cells. Int. J. Med. Sci. 2018, 15 (8), 832-839. DOI: 10.7150/ijms.23270.

NLM
He Y, Khan M, Yang J, Yao M, Yu S, Gao H. Proscillaridin A induces apoptosis, inhibits STAT3 activation and augments doxorubicin toxicity in prostate cancer cells. Int J Med Sci 2018; 15(8):832-839. doi:10.7150/ijms.23270. https://www.medsci.org/v15p0832.htm

CSE
He Y, Khan M, Yang J, Yao M, Yu S, Gao H. 2018. Proscillaridin A induces apoptosis, inhibits STAT3 activation and augments doxorubicin toxicity in prostate cancer cells. Int J Med Sci. 15(8):832-839.

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