02570nas a2200241 4500008004100000245015600041210006900197260001400266300001200280490000700292520177100299653003202070653001202102653002902114653001002143653002202153100001802175700003002193700001902223700002802242700002202270856003602292 2022 eng d00aAlpha-Mangostin Enhances Proliferation in Sorafenib-Surviving HepG2 Liver Cancer Cells by Increasing Anti-Apoptosis and Antioxidant Markers Expressions0 aAlphaMangostin Enhances Proliferation in SorafenibSurviving HepG cJune 2022 a584-5900 v143 a

Background: Sorafenib is the first-line systemic option for treatment in advanced liver cancer. However, sorafenib resistance may develop rapidly, which may involve apoptosis and oxidative stress dysregulations. Several alternative treatments have been suggested to alleviate the delayed resistance of cancer cells to sorafenib, including alpha mangostin (AM). According to an earlier study, AM might be able to overcome doxorubicin resistance in hepatocellular cancer cells. Objective: The aim of this study was to investigate the effects of AM in sorafenib-surviving HepG2 cells, a hepatocellular carcinoma (HCC) cell line. Methods: Sorafenib 10 μM was used to treat HepG2 to obtain sorafenib-surviving cells. Subsequently, sorafenib surviving cells were treated with DMSO -(vehicle) or sorafenib (SF) 10 μM or AM 20 μM, or SF 10 μM + AM 20 μM. Afterward, the cells were counted, collected and extracted for RNA. The mRNA expressions of Ki-67, c-Jun, Bcl-2, Bax, Caspase-3 and -9, GPx, and MnSOD were then quantified using qRT-PCR. Results: Treatment of alpha-mangostin, alone or in combination with sorafenib combined enhanced the expressions of proliferation markers, Ki-67 and c-Jun. In addition, there was a marked increase in mRNA expressions of Bax and BCl2, but not Caspase-3 and -9. There were amplifications of antioxidant markers expressions, GPx, and MnSOD after AM or a combination of sorafenib and AM. Conclusion: Treatment of alpha mangostin in sorafenib-surviving HCC cells caused an increase in proliferation markers, which might be explained by the reduced expressions of apoptosis markers and enhancement of antioxidant markers.

10aAnti-cancer drug resistance10aCaspase10aHepatocellular carcinoma10aKi-6710aOxidative stress.1 aLouisa, Melva1 aAnnisa, Meuthia, Faralita1 aBasuki, Pamela1 aLauren, Brigitta, Cindy1 aAdenina, Syarinta uhttps://phcogj.com/article/1805