NDLI: Downregulation of c-Met expression does not enhance the sensitivity of gastric cancer cell line MKN-45 to gefitinib.

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Downregulation of c-Met expression does not enhance the sensitivity of gastric cancer cell line MKN-45 to gefitinib.

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Downregulation of c-Met expression does not enhance the sensitivity of gastric cancer cell line MKN-45 to gefitinib.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ma, Jin-An Li, Wenjuan Zou, Fangwen Hu, Chunhong Zhou, Dongai Ren, Jing Zou, Wen Wei, Yajun Zhou, Ying
Description	Author Affiliation: Ma JA ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.); Hu C ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.); Li W ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.); Ren J ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.); Zou F ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.); Zhou D ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.); Zou W ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.); Wei Y ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.); Zhou Y ( Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.)
Abstract	The aim of the present study was to investigate the effect of downregulation of the cMet gene on signal transduction and apoptosis in gastric cancer MKN45 cells; furthermore, the study aimed to determine whether altered cMet gene expression affected MKN45 sensitivity to gefitinib. Three cMetspecific small interfering RNAs (siRNAs) were synthesized and transfected into MKN45 cells. Messenger RNA (mRNA) and protein levels of cMet and its downstream signaling molecules [phosphoinositide 3kinase (PI3K) and AKT] were examined using reverse transcription polymerase chain reaction and western blot analysis 48 h following transfection. Cell apoptosis was evaluated using AnnexinV/propidium iodide double staining and fluorescenceactivated cell sorting analysis. An MTT assay was performed in order to measure the 50% inhibitory concentration (IC50) of gefitinib on MKN45 cells. The results of the present study demonstrated that 48 h posttransfection with cMet siRNA, MKN45 cells showed significantly downregulated expression of cMet mRNA and protein as well as an increased rate of apoptosis (P<0.05). In addition, following cMet siRNA transfection mRNA and protein levels of PI3K and AKT were not significantly altered in MKN45 cells (P>0.05); however, a marked decrease in the expression levels of phosphorylated (p)PI3K and pAKT was observed (P<0.05). Furthermore, the IC50 of gefitinib in MKN45 cells was not significantly decreased. In conclusion, knockdown of the cMet gene promoted gastric cancer cell apoptosis and inhibited downstream pPI3K and pAKT; however, the sensitivity of MKN45 cells to gefitinib was not increased.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-03-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Antineoplastic Agents Pharmacology Gene Expression Regulation, Neoplastic Drug Effects Protein Kinase Inhibitors Proto-oncogene Proteins C-met Genetics Quinazolines Stomach Neoplasms Apoptosis Cell Line, Tumor Down-regulation Gene Expression Gene Silencing Inhibitory Concentration 50 Phosphatidylinositol 3-kinases Metabolism Proto-oncogene Proteins C-akt Rna Interference Rna, Messenger Signal Transduction Transfection Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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