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Updated: Feb 16, 2026

Isolation of Human Endothelial Cells from Normal Colon and Colorectal Carcinoma - An Improved Protocol
Published on: April 4, 2018
Antitumor activity of Notch‑1 inhibition in human colorectal carcinoma cells
Wangdi Liao1, Guohua Li1, Yu You1
1Department of Gastroenterology, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Abstract:
This study investigated the roles of Notch‑1 in colorectal carcinoma, to assess the mechanisms. The expression of Notch‑1 and its ligand-Jagged1 was detected in human colorectal carcinoma, colorectal adenoma, paracancerous tissue and normal colorectal tissue by immunohistochemistry. Colorectal carcinoma cell lines were utilized to confirm the expression of Notch‑1 in colorectal carcinoma cells. Lentiviral- encoding Notch‑1‑siRNA, as well as Notch‑1 inhibitor was employed to silence Notch‑1 expression and to inhibit Notch‑1 activity in HT29 cells, respectively. As evidenced, Notch‑1 and Jagged1 were highly expressed in colorectal carcinoma and colorectal adenoma tissues, compared with those in paracancerous tissue and normal colorectal tissue. However, the expression of Notch‑1 and Jagged1 was comparable in colorectal carcinoma and colorectal adenoma tissues, and in paracancerous and normal colorectal tissues. After screening colorectal carcinoma cell lines, Notch‑1 was extensively expressed in COLO 205, HT29, SW480 and SW1116 cells, but slightly expressed in LoVo cells. Subsequently, HT29 cell line was selected to investigate the roles of Notch‑1 in tumor cell growth and apoptosis. Lenti-viral encoding Notch‑1 siRNA significantly decreased Notch‑1 expression, inhibited cell growth, arrested the cell cycle at G1 phase and promoted apoptosis. These effects were further confirmed by the Notch‑1 inhibitor DAPT. Additionally, we evidenced that Notch‑1 silence promoted P21 and PUMA expression in HT29 cells. Taken together, Notch‑1 is an oncogene in colorectal carcinoma and the inhibition of Notch‑1 could delay the cell growth and promote apoptosis in colorectal cancer.
Insights
Notch-1 acts as an oncogene in colorectal cancer. Inhibiting Notch-1 expression and activity significantly reduces tumor cell growth and promotes apoptosis, offering a potential therapeutic strategy for colorectal carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- The role of Notch-1 signaling in cancer development is increasingly recognized.
- Understanding Notch-1's specific function in colorectal carcinoma is crucial for targeted therapies.
Purpose of the Study:
- To investigate the expression and functional role of Notch-1 in colorectal carcinoma.
- To explore the potential of targeting Notch-1 for cancer treatment.
Main Methods:
- Immunohistochemistry was used to detect Notch-1 and Jagged1 expression in various colorectal tissues.
- Colorectal cancer cell lines were used to confirm Notch-1 expression.
- Lentiviral-mediated Notch-1 siRNA and the Notch-1 inhibitor DAPT were employed to modulate Notch-1 activity in HT29 cells.
Main Results:
- Notch-1 and Jagged1 were significantly upregulated in colorectal carcinoma and adenoma tissues compared to normal tissues.
- Notch-1 was widely expressed in multiple colorectal cancer cell lines.
- Silencing Notch-1 inhibited cell proliferation, induced G1 cell cycle arrest, and promoted apoptosis in HT29 cells, also increasing P21 and PUMA expression.
Conclusions:
- Notch-1 functions as an oncogene in colorectal carcinoma.
- Inhibition of Notch-1 can suppress tumor cell growth and induce apoptosis, suggesting its potential as a therapeutic target in colorectal cancer.
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