RT Journal Article
SR Electronic
T1 Mangosteen Inhibits Growth and Survival of Cervical Cancer Cells
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 2903
OP 2909
DO 10.21873/anticanres.15772
VO 42
IS 6
A1 NATHAN T. GIVENS
A1 LEI ZHAO
A1 ZIWEN ZHU
A1 MARCO LEQUIO
A1 HUAPING XIAO
A1 BRADLEY D. JOHNSON
A1 QIAN BAI
A1 MARK R. WAKEFIELD
A1 YUJIANG FANG
YR 2022
UL http://ar.iiarjournals.org/content/42/6/2903.abstract
AB Background: Cervical cancer is the most common cancer of the female reproductive system. Late-stage cervical cancer treatment has been largely unsuccessful, and urgent anti-cancer therapy is needed. Mangosteen, a tropical fruit, has been studied and found to be rich in xanthones, known anti-cancer compounds. This study was designed to investigate the effect of mangosteen extract (ME) on SiHa cervical cancer cells and to explore the underlying molecular mechanisms. Materials and Methods: Clonogenic survival assay, Quick Cell Proliferation Assay, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining, and caspase-3 activity kits were used to investigate the in vitro role of ME treatment in SiHa cervical cancer cell growth. We further investigated the possible molecular mechanisms using RT-PCR. Statistical analysis was done with unpaired two-tailed Student’s t-test and significance at p-value <0.05; each experiment was repeated three times. Results: Our study found that the growth and proliferation of SiHa cervical cancer cells was inhibited by ME. ME also induced apoptosis in SiHa cervical cancer cells. The anti-proliferative effect of ME on cervical cancer cells was associated with statistically significant (p<0.05) down-regulation of the pro-proliferative molecules cyclin B, cyclin D and cyclin E. The pro-apoptotic effect of ME was associated with statistically significant (p<0.05) down-regulation of the anti-apoptotic molecules flice-like inhibitory protein (FLIP) and survivin. Conclusion: ME impedes the growth and survival of SiHa cervical cancer cells by down-regulating cyclin B, cyclin D, cyclin E as well as FLIP and survivin. ME may be a promising strategy for targeted cancer immunotherapy development.