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Suppression of stromal interaction molecule 1 inhibits SMMC7721 hepatocellular carcinoma cell proliferation by
Zhengshan Wu1, Jiangjie Qing, Yongxiang Xia
1The Liver Transplantation Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Abstract:
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.
Insights
Stromal interaction molecule 1 (STIM1) is crucial for hepatocellular carcinoma growth. Inhibiting STIM1 reduces cancer cell proliferation and DNA synthesis, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Cell Biology
- Molecular Medicine
Background:
- Stromal interaction molecule 1 (STIM1) is an endoplasmic reticulum Ca(2+) sensor involved in Ca(2+) channel activation.
- STIM1 plays a critical role in the progression of various cancers, but its function in hepatocellular carcinoma (HCC) is unknown.
Purpose of the Study:
- To investigate the role of STIM1 in the growth and development of hepatocellular carcinoma.
- To evaluate STIM1 as a potential therapeutic target for HCC.
Main Methods:
- Lentivirus-mediated short hairpin RNA (shRNA) was used to knock down STIM1 expression in SMMC7721 HCC cells.
- STIM1 overexpression was achieved using a lentiviral vector.
- Cell proliferation, colony formation, cell cycle, and DNA synthesis were assessed.
Main Results:
- Knockdown of STIM1 significantly inhibited SMMC7721 cell proliferation and colony-forming ability.
- STIM1 knockdown led to cell cycle arrest at the G0/G1 phase and decreased DNA synthesis.
- Overexpression of STIM1 promoted SMMC7721 cell proliferation.
Conclusions:
- STIM1 plays a significant role in promoting hepatocellular carcinoma cell growth.
- STIM1 represents a potential therapeutic target for hepatocellular carcinoma treatment.