2015Unpublished venueRequires access

Sorafenib reverses resistance of gastric cancer to treatment by cisplatin through down-regulating MDR1 expression

Yi-sheng HuangZhi, Xuehua Zhang

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Abstract

Cisplatin (DDP) has been successfully used in the treatment of gastric cancer; however, resistance of gastric tumors to cisplatin has also resulted in frequent treatment failure. To investigate the effect of sorafenib in reversing the resistance of human gastric cancer cell line SGC7901/DDP to treatment by cisplatin, and to examine possible underlying mechanisms. A SGC7901/DDP cell line was treated with different concentrations of sorafenib, with and without cisplatin. The reversing ability of so- rafenib on cisplatin treatment was examined using MTT, FACS, and xenograft models. Western blotting and immunofluorescence were used to determine expressions of MDR1, p-Akt, and p-ERK. Sorafenib inhibited prolifera- tion of human gastric cancer cell line SGC7901/DDP, both when used alone and in combination with cisplatin. Expression levels of MDR1, p-Akt, and p-ERK were sig- nificantly decreased after sorafenib treatment. Sorafenib may reverse resistance of human gastric cancer cell line SGC7901/DDP to cisplatin through down-regulating MDR1 expression.

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What this paper is about

Cisplatin (DDP) has been successfully used in the treatment of gastric cancer; however, resistance of gastric tumors to cisplatin has also resulted in frequent treatment failure. To investigate the effect of sorafenib in reversing the resistance of human gastric cancer cell line SGC7901/DDP to treatment by cisplatin, and to examine possible underlying mechanisms. A SGC7901/DDP cell line was treated with different concentrations of sorafenib, with and without cisplatin. The reversing ability of so- rafenib on cisplatin treatment was examined using MTT, FACS, and xenograft models. Western blotting and immunofluorescence were used to determine expressions of MDR1, p-Akt, and p-ERK. Sorafenib inhibited prolifera- tion of human gastric cancer cell line SGC7901/DDP, both when used alone and in combination with cisplatin. Expression levels of MDR1, p-Akt, and p-ERK were sig- nificantly decreased after sorafenib treatment. Sorafenib may reverse resistance of human gastric cancer cell line SGC7901/DDP to cisplatin through down-regulating MDR1 expression.

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Available abstract

Cisplatin (DDP) has been successfully used in the treatment of gastric cancer; however, resistance of gastric tumors to cisplatin has also resulted in frequent treatment failure. To investigate the effect of sorafenib in reversing the resistance of human gastric cancer cell line SGC7901/DDP to treatment by cisplatin, and to examine possible underlying mechanisms. A SGC7901/DDP cell line was treated with different concentrations of sorafenib, with and without cisplatin. The reversing ability of so- rafenib on cisplatin treatment was examined using MTT, FACS, and xenograft models. Western blotting and immunofluorescence were used to determine expressions of MDR1, p-Akt, and p-ERK. Sorafenib inhibited prolifera- tion of human gastric cancer cell line SGC7901/DDP, both when used alone and in combination with cisplatin. Expression levels of MDR1, p-Akt, and p-ERK were sig- nificantly decreased after sorafenib treatment. Sorafenib may reverse resistance of human gastric cancer cell line SGC7901/DDP to cisplatin through down-regulating MDR1 expression.

Key concepts: Cisplatin, Sorafenib, Cancer, Cancer research, MAPK/ERK pathway, Medicine, MTT assay, Cancer cell

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