Abstract: OBJECTIVE： To investigate the regulatory mechanism of oncogene BCR/ABL fusion gene on PTEN signaling pathway in proliferation and apoptosis of K562 cells in vitro. METHODS: To detect the mRNA levels of BCR/ABL, PTEN and mTOR in K562 cells treated with different concentrations of Imatinib by real-time fluorescent relative- quantification reverse transcriptional PCR (FQ-PCR) and the protein levels of Akt, p-Akt by Western blotting technique. RESULTS: The expression level of PTEN mRNA was up-regulated and the mTOR mRNA was down-regulated with the reduction of BCR/ABL fusion gene in the initial 36 h after 1 μg/ml imatinib inhibiting K562 cells. Then the PTEN mRNA decreased and the mTOR mRNA expression restored, but the p-Akt was continuously down-regulated with the restoration of BCR/ABL fusion gene 48 h later. BCR/ABL and PTEN mRNA showed a positive correlation; whilst BCR/ABL had a negative correlation with mTOR mRNA and p-Akt protein. CONCLUSION: BCR/ABL fusion gene could regulate p-Akt, mTOR pathway by inhibiting PTEN expression in K562 cells and affected cell proliferation, apoptosis and cell cycle.

Key words: BCR/ABL fusion gene, PTEN, mTOR, Akt