Related Experiment Video
Updated: May 6, 2026
Orthotopic Implantation of Patient-Derived Cancer Cells in Mice Recapitulates Advanced Colorectal Cancer
Published on: February 10, 2023
P7 peptides targeting bFGF sensitize colorectal cancer cells to CPT-11
Wu Luo1, Yonglin Yu, Ruixue Wang
1Institute of Tissue Transplantation and Immunology, Jinan University, Guangzhou, Guangdong, P.R. China.
Abstract:
The low survival rate of patients with colorectal cancer (CRC) is mainly due to the drug resistance of tumor cells to chemotherapeutic agents. It has been reported that basic fibroblast growth factor (bFGF) is an essential factor involved in the epigenetic mechanisms of drug resistance, which provides a novel potential target for improving the sensitivity of tumor cells to chemotherapeutic agents. In this study, we first demonstrate that a novel bFGF antagonist, peptide P7, previously isolated by phage display technology, reversed bFGF-induced resistance to irinotecan hydrochloride (CPT-11), and counteracted the anti-apoptotic effects of bFGF on CPT-11-treated HT-29 cells. Further experiments indicated that the inhibition of Akt activation, the suppression of bFGF internalization, the increase in the Bax to Bcl-2 ratio and the downregulation of cytokeratin 8 (CK8) by P7 may contribute to the counteracting of the anti-apoptotic effects of bFGF, and further reversal of bFGF-induced resistance to CPT-11. Our results suggest that peptide P7 may have therapeutic potential in CRC as a sensitizer to chemotherapeutic agents by targeting bFGF.
Insights
A novel peptide, P7, targets basic fibroblast growth factor (bFGF) to overcome drug resistance in colorectal cancer (CRC). This peptide sensitizes cancer cells to chemotherapy by counteracting bFGF
Area of Science:
- Oncology
- Molecular Biology
- Drug Discovery
Background:
- Colorectal cancer (CRC) survival rates are low due to tumor cell drug resistance.
- Basic fibroblast growth factor (bFGF) plays a role in epigenetic mechanisms of drug resistance.
- Targeting bFGF offers a potential strategy to enhance chemotherapy sensitivity.
Purpose of the Study:
- To investigate the efficacy of a novel bFGF antagonist, peptide P7, in overcoming chemoresistance in CRC.
- To elucidate the molecular mechanisms by which peptide P7 reverses bFGF-induced drug resistance.
Main Methods:
- Phage display technology was used to isolate peptide P7.
- Experiments involved treating HT-29 cells with irinotecan hydrochloride (CPT-11) and peptide P7.
- Assays measured Akt activation, bFGF internalization, apoptosis markers (Bax, Bcl-2), and cytokeratin 8 (CK8) expression.
Main Results:
- Peptide P7 reversed bFGF-induced resistance to CPT-11 in HT-29 cells.
- P7 counteracted the anti-apoptotic effects of bFGF.
- Mechanistically, P7 inhibited Akt activation, suppressed bFGF internalization, increased the Bax/Bcl-2 ratio, and downregulated CK8.
Conclusions:
- Peptide P7 demonstrates potential as a therapeutic agent to sensitize colorectal cancer cells to chemotherapy.
- Targeting bFGF with peptide P7 offers a promising strategy to improve CRC treatment outcomes.
More Related Videos
09:29Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
Published on: September 30, 2016
10:26Biotinylated Cell-penetrating Peptides to Study Intracellular Protein-protein Interactions
Published on: December 20, 2017
Related Concept Videos
02:38Mitogens and the Cell Cycle
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...