[The effects and mechanisms of BTBD10 on the proliferation of islet beta cell]

To explore the role of BTBD10 overexpression in the proliferation of insulinoma cell line INS-1 and its mechanism.

The recombined expression plasmid of pcDNA4.0-BTBD10 was constructed by gene cloning technique and was transfected into INS-1 cell by lipofectamine 2000. The stable overexpression BTBD10 of INS-1 cell was selected at 48(th) hour after transfection. INS-1 cell proliferation activity was measured by MTT method. The expression of BTBD10, protein kinase B (Akt), phospho-Akt (p-Akt), mammal target of rapamycin (mTOR) and phospho-mTOR (p-mTOR) were determined by Western blot.

The stable overexpression BTBD10 of INS-1 cell was successfully constructed. Overproduction of BTBD10 promoted beta cell proliferation. The phosphorylation of Akt and mTOR was increased and the ratio of p-Akt/Akt and p-mTOR/mTOR was enhanced in the INS-1 overexpressed by BTBD10. But the expression of total Akt and mTOR presented no obvious changes.

The overexpression BTBD10 of INS-1 cell could activate of Akt/mTOR signalling pathway via stimulating phospho-mTOR and Akt, and enhance overall cell protein translation, so as to promote proliferation of INS-1 cell.