Suppression of stromal interaction molecule 1 inhibits SMMC7721 hepatocellular carcinoma cell proliferation by inducing cell cycle arrest.

Stromal interaction molecule 1 (STIM1), an endoplasmic reticulum luminal Ca(2+) sensor, activates Ca(2+) -release-activated Ca(2+) channels and migrates from the Ca(2+) store to the plasma membrane. Recently, STIM1 was shown be critical for the progression of several cancers, including breast cancer and cervical cancer. However, its role in hepatocellular carcinoma has remained unknown. The current study was aimed to evaluate the effect of STIM1 on the growth of hepatocellular cancer. Lentivirus-mediated short hairpin RNA targeting STIM1 was transduced into SMMC7721 cells to knock down STIM1 expression. Knockdown of STIM1 significantly inhibited cell proliferation and colony-forming ability and arrested the cell cycle at the G0/G1 phase. Moreover, the DNA synthesis progression was also decreased. Furthermore, lentiviral vector-mediated overexpression of STIM1 promoted the proliferation of SMMC7721 cells. Our findings suggest that STIM1 may play an important role in the development of hepatocellular cancer and may be a potential target for therapy.