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Updated: Jan 31, 2026
A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
Published on: July 6, 2017
Effect of RSK4 on biological characteristics of colorectal cancer
Qingqing Ye1, Xuan Wang2, Min Jin3
1Department of Breast Surgery, First Affiliated Hospital of Yangtze University, Jingzhou, 434000, Hubei, China.
Background:
This study aimed to investigate the expression of P90 Ribosomal Protein S6 kinase 4 (RSK4) in colorectal cancer cells and its biological function.
Methods:
We selected early SW480 and HCT116 colorectal cancer cell lines, using Lipofectamine™ 2000 transfection reagent carrying RSK4 gene transfected into cells to establish the colorectal cancer cell lines with high expression of RSK4. RT-PCR and western blot (WB) analysis confirmed RSK4 expression in SW480 and HCT116 cancer cell lines. We used methylthiazoltetrazolium (MTT) assay and flow cytometry to detect the proliferation of colorectal cancer cells. After transfection of RSK4, the effect of RSK4 on the RNA levels associated with epithelial-mesenchymal transition (EMT) of colorectal cancer cells was analyzed by real-time fluorescence quantitative PCR and the expression of EMT-related protein was detected by WB analysis.
Results:
After transfection of RSK4 overexpression, the MTT assay detected that RSK4 could significantly inhibit the growth of colorectal cancer cells in vitro; flow cytometry detected that S-phase cells decreased significantly, and G0/1 cells increased significantly (P < 0.05). The invasion ability of SW480 and HCT116 cells transfected with RSK4 was markedly lower than that in the control group, and the difference was statistically significant (P < 0.05). Fluorescent quantitative PCR and WB analysis showed that the expression of EMT-associated molecular E-cadherin was remarkably increased and the expression of Snail was significantly decreased (P < 0.01).
Conclusion:
RSK4 gene in colorectal cancer cell lines with low expression of RSK4 after transfection can inhibit the growth and invasion of tumor cells. RSK4 gene may inhibit EMT and inhibit metastasis of colorectal cancer cells, may be a potential tumor suppressor gene and inhibit tumor distant metastasis, and may provide the biological basis for new therapeutic targets.
Insights
The P90 Ribosomal Protein S6 kinase 4 (RSK4) gene inhibits colorectal cancer cell growth and invasion. RSK4 may suppress epithelial-mesenchymal transition (EMT), indicating its potential as a therapeutic target for colorectal cancer metastasis.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Biology
Background:
- Colorectal cancer (CRC) is a significant global health concern.
- Understanding the molecular mechanisms underlying CRC progression is crucial for developing effective treatments.
- The role of P90 Ribosomal Protein S6 kinase 4 (RSK4) in CRC remains to be fully elucidated.
Purpose of the Study:
- To investigate the expression of RSK4 in colorectal cancer cells.
- To determine the biological function of RSK4 in CRC cell proliferation, invasion, and epithelial-mesenchymal transition (EMT).
Main Methods:
- RSK4 gene was transfected into SW480 and HCT116 colorectal cancer cell lines.
- RSK4 expression was confirmed using RT-PCR and Western Blot (WB).
- Cell proliferation was assessed by MTT assay and flow cytometry.
- EMT markers were analyzed by real-time fluorescence quantitative PCR and WB.
Main Results:
- RSK4 overexpression significantly inhibited colorectal cancer cell growth in vitro.
- RSK4 transfection led to a decrease in S-phase cells and an increase in G0/1 phase cells.
- RSK4 significantly reduced cell invasion and suppressed EMT markers, increasing E-cadherin and decreasing Snail expression.
Conclusions:
- RSK4 inhibits the growth and invasion of colorectal cancer cells.
- RSK4 may act as a tumor suppressor by inhibiting EMT and metastasis.
- RSK4 presents a potential therapeutic target for colorectal cancer treatment and metastasis inhibition.
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