Dian-dian Chen1, Lin-chun Feng1, Rui Ye2, Yu-qi He, Ya-di Wang. 1. Department of Radiation Oncology,Chinese PLA General Hospital,Beijing 100853,China2Department of Oncology,Beidaihe Sanatorium of Beijing Military Command,Qinhuangdao,Hebei 066100,China3Department of Gastroenterology,4Department of Radiation Oncology,General Hospital of Beijing Military Command,Beijing 100700,China. 2. 1. Department of Radiation Oncology,Chinese PLA General Hospital,Beijing 100853,China2Department of Oncology,Beidaihe Sanatorium of Beijing Military Command,Qinhuangdao,Hebei 066100,China3Department of Gastroenterology,4Department of Radiation Oncology,General Hospital of Beijing Military Command,Beijing 100700,China;
Abstract
OBJECTIVE: To investigate the regulatory effect of miR-29b on gastric cells' resistance to cisplatin. METHODS: The expression of miR-29b in gastric cancer cell line treated with cisplatin concentration gradient was detected using quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blotting. CCK8 was used to measure the cell viability after cisplatin treatment in condition of miR-29b knock-down and overexpression. RESULTS: The expression of miR-29b was significantly upregualted by cisplatin treatment,while its target gene AKT2 was downregulated. The up-regulation of miR-29b enhanced the sensitivity of gastric cancer cells to cisplatin,while the knock-down of miR-29b enhanced the cisplatin resistance. Rescue experiments demonstrated that the miR-29b might regulate cisplatin resistance of gastric cancer cell by targeting PI3K/Akt pathway. The expressions of the other two members of miR-29 family, miR-29a/c, were promoted by cisplatin treatment,but they had no significant effect on gastric cancer cell's resistance to cisplatin. CONCLUSION: miR-29b can enhance the sensitivity of S gastric cancer cell by directly targeting PI3K/Akt pathway.
OBJECTIVE: To investigate the regulatory effect of miR-29b on gastric cells' resistance to cisplatin. METHODS: The expression of miR-29b in gastric cancer cell line treated with cisplatin concentration gradient was detected using quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blotting. CCK8 was used to measure the cell viability after cisplatin treatment in condition of miR-29b knock-down and overexpression. RESULTS: The expression of miR-29b was significantly upregualted by cisplatin treatment,while its target gene AKT2 was downregulated. The up-regulation of miR-29b enhanced the sensitivity of gastric cancer cells to cisplatin,while the knock-down of miR-29b enhanced the cisplatin resistance. Rescue experiments demonstrated that the miR-29b might regulate cisplatin resistance of gastric cancer cell by targeting PI3K/Akt pathway. The expressions of the other two members of miR-29 family, miR-29a/c, were promoted by cisplatin treatment,but they had no significant effect on gastric cancer cell's resistance to cisplatin. CONCLUSION:miR-29b can enhance the sensitivity of S gastric cancer cell by directly targeting PI3K/Akt pathway.
Authors: Penn Muluhngwi; Abirami Krishna; Stephany L Vittitow; Joshua T Napier; Kirsten M Richardson; Mackenzie Ellis; Justin L Mott; Carolyn M Klinge Journal: Cancer Lett Date: 2016-12-13 Impact factor: 8.679
Authors: A K M Nawshad Hossian; Fatema Tuz Zahra; Sagun Poudel; Camille F Abshire; Paula Polk; Jone Garai; Jovanny Zabaleta; Constantinos M Mikelis; George Mattheolabakis Journal: Sci Rep Date: 2021-03-22 Impact factor: 4.379