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Effects of the downregulation of SnoN expression on HepG2 cell proliferation and apoptosis
Wenqi Wang1, Changhong Liu, Yiguo Wang
1Department of Gastroenterology, Qianfoshan Hospital Affiliated to Shandong University, Jinan, Shandong 250014, P.R. China. wangwq62@163.com
Abstract:
Ski‑novel protein (SnoN) is a proto‑oncogene that belongs to the Ski protein family and is involved in regulating processes such as cell proliferation and apoptosis. To investigate the role of SnoN in the proliferation and apoptosis of HepG2 cells, we downregulated its expression by the use of small interfering RNA (siRNA). Three fragments predicted to have RNAi capacity were designed and synthesized as the target siRNAs (siRNA‑A, ‑B and ‑C). Following transfection, inhibition efficiency was detected by reverse transcription PCR (RT‑PCR) and western blot analysis. The siRNA with the optimal inhibition efficiency was used for the cell proliferation and apoptosis analysis. Cell proliferation was analyzed by the Cell Counting Kit‑8 (CCK‑8) and cell apoptosis was investigated by flow cytometry. In our study, all three siRNAs efficiently inhibited SnoN expression, and siRNA‑C demonstrated the optimal inhibition efficiency. We found that following downregulation of SnoN expression, HepG2 cell proliferation was significantly inhibited (P<0.05), while HepG2 cell apoptosis was significantly increased (P<0.05). SnoN‑specific siRNA is capable of effectively inhibiting the expression of SnoN in human HepG2 cells, and the downregulation of SnoN expression induces growth inhibition and apoptosis.
Insights
Ski‑novel protein (SnoN) downregulation inhibits HepG2 cell proliferation and induces apoptosis. SnoN-specific small interfering RNA (siRNA) effectively reduces SnoN expression, offering a potential therapeutic strategy.
Area of Science:
- Molecular Biology
- Oncology
Background:
- Ski‑novel protein (SnoN) is a proto‑oncogene implicated in cell growth and programmed cell death.
- Understanding SnoN's role in hepatocellular carcinoma (HCC) is crucial for targeted therapies.
Purpose of the Study:
- To investigate the functional role of SnoN in HepG2 cell proliferation and apoptosis.
- To evaluate the efficacy of small interfering RNA (siRNA) in downregulating SnoN expression in HepG2 cells.
Main Methods:
- Three siRNAs targeting SnoN were designed and synthesized.
- Inhibition efficiency was assessed using reverse transcription PCR (RT-PCR) and western blot.
- Cell Counting Kit-8 (CCK-8) and flow cytometry were employed for proliferation and apoptosis analyses.
Main Results:
- All synthesized siRNAs effectively inhibited SnoN expression, with siRNA-C showing optimal efficiency.
- Downregulation of SnoN significantly inhibited HepG2 cell proliferation (P<0.05).
- Significant induction of HepG2 cell apoptosis was observed following SnoN downregulation (P<0.05).
Conclusions:
- SnoN-specific siRNA is effective in inhibiting SnoN expression in human HepG2 cells.
- Downregulation of SnoN induces significant growth inhibition and apoptosis in HepG2 cells.
- Targeting SnoN represents a promising strategy for HCC treatment.
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