Silence of p15 expression by RNAi enhances cisplatin resistance in hepatocellular carcinoma cells
Autor: | Yuanhong Guo, Zhenshuang Zhu, Weiqing Chen, Dianliang Fang |
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Rok vydání: | 2012 |
Předmět: |
inorganic chemicals
Carcinoma Hepatocellular Cell Antineoplastic Agents Biology p15 Flow cytometry RNA interference medicine Humans Gene silencing Cyclin-Dependent Kinase Inhibitor p15 Cisplatin lcsh:R5-920 Gene knockdown drug resistance medicine.diagnostic_test Liver Neoplasms hepatocellular carcinoma Hep G2 Cells General Medicine Cell cycle medicine.disease Molecular biology digestive system diseases Gene Expression Regulation Neoplastic medicine.anatomical_structure Drug Resistance Neoplasm Hepatocellular carcinoma cell cycle RNA Interference lcsh:Medicine (General) Research Article medicine.drug |
Zdroj: | Bosnian Journal of Basic Medical Sciences, Vol 12, Iss 1 (2012) |
ISSN: | 1840-4812 1512-8601 |
DOI: | 10.17305/bjbms.2012.2523 |
Popis: | The insensitivity of hepatocellular carcinoma to chemotherapy is associated with alternation in tumor cell cycling. This current study was designed to investigate the impact of p15 silencing on the sensitivity of Human hepatocellular carcinoma HepG2 cells to cisplatin. HepG2/CDDP/1.6 and HepG2/CDDP/2.0 cells were induced by culture with increased doses of cisplatin and their sensitivities to cis-Diamine dichloroplatinum (CDDP) were determined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). The impacts of p15 silencing on the cell cycling and P-gp expression were characterized by flow cytometry, RT-PCR and Western blot assays, respectively. Knockdown of p15 expression dramatically reduced the relative levels of p15 expression and the frequency of phase G1, promoting cell cycling. On the other hand, knockdown of p15 expression significantly up-regulated the expression of P-glycoprotein (P-gp) in HepG2/CDDP/2.0 cells, associated with the increased resistance of HepG2 cells to CDDP in vitro. In conclusion, the p15 may be a critical regulator of the development of CDDP resistance in HepG2 cells. |
Databáze: | OpenAIRE |
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