Imatinib induces up-regulation ofNM23, a metastasis suppressor gene, in human Hepatocarcinoma (HepG2) Cell Line.
OBJECTIVE
The present study investigated the anti-tumor activity of Imatinib mesylate through modulation ofNM23gene expression in human hepatocellular carcinoma (HepG2) cell line.


BACKGROUND
Hepatocellular carcinoma (HCC) is considered to be the third leading cause of cancer related death worldwide. Down regulation ofNM23, a metastasis suppressor gene, has been associated with several types of malignant cancer. Recently, effects of Imatinib mesylate, a first member of tyrosine kinases inhibitors, were indicated in research and treatment of different malignant tumors.


METHODS
Cell viability was quantitated by MTT assay after HepG2 cells exposure to Imatinib mesylate at various concentrations of 0, 1.56, 3.125, 6.25, 12.5, 25,50μM for 24 hours. Also, quantitative real time PCR technique was applied for the detection ofNM23gene expression in HepG2 cell line.


RESULTS
There was a dose dependent increase in the cytotoxicity effect of imatinib. The real time PCR results demonstrated that inhibitory effect of Imatinib mesylate on viability via up regulation ofNM23gene expression compared toGAPDHgene (internal control gene) in cancer cells.


CONCLUSIONS
According to our findings, imatinib can modulate metastasis by enhancingNm23gene expression in human hepatocellular carcinoma (HepG2) cell line.
Department of Genetics and Biotechnology, School of Biological Science, Varamin-Pishva Branch, Islamic Azad University, Varamin, Iran.
Behta
B
Keshavarz-Pakseresht
Young Researchers and Elite Club, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Seyed Ataollah Sadat
SA
Shandiz
Department of Genetics and Biotechnology, School of Biological Science, Varamin-Pishva Branch, Islamic Azad University, Varamin, Iran.
Fahimeh
F
Baghbani-Arani
HepG2; Imatinib mesylate; NM23; metastasis