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Effect of Combined Sorafenib/Cisplatinum Treatment on the Autophagy and Proliferation of Hepatocellular Carcinoma hepG2 Cells in Vitro

OBJECTIVE: To explore the effect of combined Sorafenib/ cisplatinum treatment on the autophagy and proliferation of hepatocellular carcinoma (HepG2) cells in vitro. METHODS: HepG2 cells were cultured and treated with different concentrations of Sorafenib, cisplatinum, or a combination of both over a...

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Detalles Bibliográficos
Autores principales: Wang, Yaoting, Wang, Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: West Asia Organization for Cancer Prevention 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7798144/
https://www.ncbi.nlm.nih.gov/pubmed/33112540
http://dx.doi.org/10.31557/APJCP.2020.21.10.2853
Descripción
Sumario:OBJECTIVE: To explore the effect of combined Sorafenib/ cisplatinum treatment on the autophagy and proliferation of hepatocellular carcinoma (HepG2) cells in vitro. METHODS: HepG2 cells were cultured and treated with different concentrations of Sorafenib, cisplatinum, or a combination of both over a 24-hour period. Cell proliferation was evaluated using a CCK8 assay, and the mRNA expression of the autophagy-related proteins AKT, mTOR, and LC3 were detected using quantitative PCR (qPCR). AKT, pAKT (Ser473), mTOR, pmTOR (Ser2448), LC3I, and LC3II protein expression levels were evaluated by western blot. RESULTS: We found that the survival rate of HepG2 cells was 47.42% when treated with Sorafenib (10 μmol/L) monotherapy, and 46.04% when treated with cisplatinum (10 mg/L) monotherapy. When Sorafenib(10 μmol/L) was combined with cisplatinum (10 mg/L), the cellular proliferation and survival rate was only 16.71% ( P <0.05). qPCR and western blot revealed that a combination of Sorafenib (10 μmol/L) and cisplatinum (10 mg/L) reduced the transcription and protein expression of autophagy-related AKT and mTOR but increased that of LC3 (P <0.05). CONCLUSION: Combining Sorafenib and cisplatinum can effectively induce cell autophagy and reduce cellular proliferation via the PI3K/AKT/mTOR signal pathway.