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Promising Modulatory Effects of Cenicriviroc on the Progression of Mouse Colorectal Cancer through Inhibition of
Mina Eslami1, Farid Azizi Jalilian1, Rezvan Najafi1
1Molecular Medicine Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Abstract:
The study was designed to assay the efficacy of cenicriviroc (CVC) on the progression of mouse colorectal cancer by downregulation of CCR2_CCL2. In this study, CVC was used to inhibit the CCR2 receptor. Next, an MTT assay was performed to evaluate the cytotoxic effects of CVC on the CT26 cell line. CT26 cells were implanted subcutaneously in BALB/c mice. After tumor implantation, one group of animals received 20 mg/kg of CVC several times. The mRNA levels of CCR2, CCL2, VEGF, NF-κB, c-Myc, vimentin, and IL33 were determined in the CT26 cell line and then tumor tissues (after 21 days), by qRT-PCR. Protein levels of the above-mentioned targets were determined by western blot and ELISA. Flow cytometry was performed to assess the changes in apoptosis. Tumor growth inhibition was measured on the 1st, 7th, and 21st days after the first treatment. In both cell line and tumor cells treated with CVC, expression levels of the markers of our interest in mRNA and protein levels were significantly reduced compared to controls. A significantly higher apoptotic index was observed in CVC-treated groups. The rates of tumor growth were significantly decreased on the 7th and 21st days after the first injection. To our knowledge, this was the first time that we demonstrated the promising effect of CVC on the development of CRC through inhibition of the CCR2_CCL2 signaling and its downstream biomarkers.
Insights
Cenicriviroc (CVC) effectively inhibited colorectal cancer (CRC) progression in mice by downregulating CCR2-CCL2 signaling. This treatment significantly reduced tumor growth and increased apoptosis, highlighting CVC
Area of Science:
- Oncology
- Immunology
- Pharmacology
Background:
- Colorectal cancer (CRC) remains a significant global health challenge.
- The CCR2-CCL2 signaling pathway plays a crucial role in tumor progression and metastasis.
- Targeting specific molecular pathways offers a promising strategy for CRC treatment.
Purpose of the Study:
- To evaluate the efficacy of cenicriviroc (CVC) in inhibiting colorectal cancer (CRC) progression in a mouse model.
- To investigate the effect of CVC on the CCR2-CCL2 signaling pathway and its downstream targets.
- To assess the impact of CVC on tumor growth, apoptosis, and key molecular markers.
Main Methods:
- In vitro cytotoxicity assessment of CVC on CT26 colon cancer cells using MTT assay.
- In vivo study involving subcutaneous implantation of CT26 cells in BALB/c mice, followed by CVC administration.
- Quantitative real-time PCR (qRT-PCR), Western blot, and ELISA were used to determine mRNA and protein expression levels of key markers (CCR2, CCL2, VEGF, NF-κB, c-Myc, vimentin, IL33).
- Flow cytometry was employed to analyze apoptosis.
- Tumor growth inhibition was measured at multiple time points.
Main Results:
- CVC treatment significantly reduced the expression of CCR2, CCL2, VEGF, NF-κB, c-Myc, vimentin, and IL33 at both mRNA and protein levels in CT26 cells and tumor tissues.
- A significant increase in the apoptotic index was observed in CVC-treated groups.
- CVC administration led to a significant decrease in tumor growth rates on days 7 and 21 post-treatment.
Conclusions:
- Cenicriviroc (CVC) demonstrates significant anti-tumor efficacy against colorectal cancer in a preclinical mouse model.
- The therapeutic effect of CVC is associated with the downregulation of the CCR2-CCL2 signaling pathway and its downstream biomarkers.
- This study provides the first evidence of CVC's potential in combating CRC development via targeted pathway inhibition.
