TY - JOUR T1 - Mangosteen Inhibits Growth and Survival of Cervical Cancer Cells JF - Anticancer Research JO - Anticancer Res SP - 2903 LP - 2909 DO - 10.21873/anticanres.15772 VL - 42 IS - 6 AU - NATHAN T. GIVENS AU - LEI ZHAO AU - ZIWEN ZHU AU - MARCO LEQUIO AU - HUAPING XIAO AU - BRADLEY D. JOHNSON AU - QIAN BAI AU - MARK R. WAKEFIELD AU - YUJIANG FANG Y1 - 2022/06/01 UR - http://ar.iiarjournals.org/content/42/6/2903.abstract N2 - 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. ER -