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Inhibition of Multifunctional Protein p32/C1QBP Promotes Cytostatic Effects in Colon Cancer Cells by Altering
Carlos Alejandro Egusquiza-Alvarez1, Angela Patricia Moreno-Londoño1, Eduardo Alvarado-Ortiz1
1Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Mexico City 04510, Mexico.
International Journal of Molecular Sciences
|March 13, 2024
Summary
The small molecule M36 inhibits the cancer-promoting protein C1QBP, reducing colon cancer cell viability and proliferation. This cytostatic effect suggests M36 as a potential therapeutic for colon cancer by targeting C1QBP.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- The protein p32 (C1QBP) is overexpressed in many cancers, including colon cancer, and is linked to poor patient survival.
- C1QBP promotes colon cancer cell migration, chemoresistance, clonogenic, and tumorigenic capacity.
- Mechanisms of C1QBP function and the impact of its inhibitors are not fully understood.
Purpose of the Study:
- To investigate the effects of a specific C1QBP inhibitor, M36, on colon cancer cell behavior.
- To explore the underlying mechanisms of C1QBP inhibition, including its impact on cellular pathways and mitochondria.
Main Methods:
- Treatment of colon cancer cell lines with the small molecule M36 in a dose-dependent manner.
- Assessment of cell viability, proliferation, and clonogenic capacity.
- Analysis of Akt-mTOR and MAPK signaling pathways.
- Evaluation of mitochondrial integrity and dynamics.
Main Results:
- M36 significantly decreased colon cancer cell viability, proliferation, and clonogenic capacity.
- The inhibitor's effects were cytostatic, not cytotoxic, reducing Akt-mTOR and MAPK pathway activation.
- M36 treatment disrupted mitochondrial integrity and dynamics in cancer cells.
Conclusions:
- C1QBP is a crucial oncogene target in colon cancer.
- The small molecule M36 demonstrates potential as a therapeutic agent for colon cancer by inhibiting C1QBP.
- M36 impacts colon cancer progression by affecting cell proliferation and mitochondrial homeostasis.
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