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Updated: Feb 19, 2026

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
Published on: July 22, 2020
[Antisense to CDK4 inhibits the growth of human colon cancer cells HT29]
Ying-jiang Ye1, Xue-guang Zhu, Shan Wang
1Surgical Oncology Laboratory, People's Hospital Peking University, Beijing 100044, China.
Objective:
Antisense CDK4 was transfected into human colorectal cancer cells HT29 to examine the effect of it on the growth and proliferation of HT29 cells.
Methods:
Antisense CDK4 transfected the HT29 cells with lipofectamine. The transfected effects were verified by the Northern blot, Western blot, morphological method, flow cell measure, etc.
Results:
The transformant cells showed the expression of exogenous antisense CDK4 mRNA, and downmodulation of endogenous CDK4 mRNA expression and inhibition of its protein synthesis. The transformant cells exhibited the partial reversion of the malignant phenotype and behavior, and that the cell growth and the ability of colony formation in soft agar were inhibited. The arrest of G1 phase was also revealed. the apoptosis rate is higher in HT29-asCDK4.
Conclusion:
The antisense CDK4 gene can inhibited the cell growth and proliferation, and induce the cell apoptosis. It might provide a new way to gene therapy of the colorectal carcinoma.
Insights
Antisense CDK4 gene therapy effectively inhibited colorectal cancer cell growth and proliferation. This approach also induced cancer cell apoptosis, offering a potential new treatment strategy for colorectal carcinoma.
Area of Science:
- Molecular biology
- Cancer research
- Gene therapy
Context:
- Colorectal cancer (CRC) remains a significant global health challenge.
- Understanding the molecular mechanisms driving CRC proliferation is crucial for developing targeted therapies.
- Cyclin-dependent kinase 4 (CDK4) plays a key role in cell cycle regulation and is implicated in various cancers.
Purpose:
- To investigate the therapeutic potential of antisense CDK4 in inhibiting the growth and proliferation of human colorectal cancer cells (HT29).
- To evaluate the impact of antisense CDK4 transfection on cellular phenotype, cell cycle progression, and apoptosis in HT29 cells.
Summary:
- HT29 cells were transfected with antisense CDK4 using lipofectamine, with transfection efficiency confirmed by molecular and cellular assays.
- Transfected cells demonstrated successful expression of antisense CDK4 mRNA, leading to down-regulation of endogenous CDK4 mRNA and protein synthesis.
- These molecular changes resulted in a partial reversion of the malignant phenotype, inhibition of cell growth and soft agar colony formation, G1 phase arrest, and increased apoptosis.
Impact:
- Antisense CDK4 effectively suppresses colorectal cancer cell growth and proliferation.
- The induction of apoptosis by antisense CDK4 presents a promising avenue for gene therapy in colorectal carcinoma.
- This study provides a foundation for developing novel targeted gene-based treatments for colorectal cancer.
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