Repurposing Statins: Exploring Anti-Tumor Effects in Colorectal Cancer
Dec 3, 2025
Colorectal cancer is a leading cause of cancer deaths, prompting researchers to explore repurposing existing drugs like statins for treatment. Discover how statins may suppress the Wnt/β-catenin signaling pathway, a key driver of tumor growth. The study reveals that statins downregulate the SATB1 protein while increasing SATB2, influencing cancer cell behavior. Additionally, statins showed promise in disrupting tumor structure and reducing growth in lab models. Tune in for insights on the potential clinical implications and future research directions!
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insights INSIGHT
Cholesterol Fuels Tumor Growth
Elevated cholesterol may support tumor growth by fueling membrane synthesis and metabolism in dividing cells.
This biological link provides a rationale for testing cholesterol-lowering drugs in CRC therapy.
insights INSIGHT
Multi-Omics Reveals Statin Effects
Researchers used multi-omics (lipidomics, transcriptomics, proteomics) plus 3D tumor models to trace statin effects across cellular layers.
This integrative approach linked cholesterol reduction to pathway and protein-level changes relevant to CRC progression.
insights INSIGHT
Statins Modulate WNT Signaling And SATB Proteins
Statins suppressed WNT/β-catenin signaling and altered SATB1/SATB2 protein dynamics in CRC cells.
The drugs lowered SATB1 (oncogenic) and increased SATB2 (tumor-suppressive), shifting cells toward an epithelial phenotype.
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Colorectal cancer (CRC) remains the second leading cause of cancer-related deaths globally. While early detection significantly improves outcomes, many patients are diagnosed at advanced stages when treatment options are limited and relapse is common. To address this challenge, researchers are exploring whether existing drugs can be repurposed for cancer therapy, a strategy that could accelerate drug development while reducing associated costs and risks.
One class of drugs under investigation is statins, commonly prescribed to reduce cholesterol and prevent cardiovascular disease. Several studies have observed a potential link between elevated cholesterol and increased CRC risk. Cholesterol may support tumor growth by promoting membrane synthesis and energy metabolism in rapidly dividing cells.
Building on this connection, researchers from leading Indian institutions, including the Indian Institute of Science Education and Research and the Center of Excellence in Epigenetics at Shiv Nadar Institution of Eminence, investigated how statins influence CRC cells at the molecular level. Their goal was to determine whether these widely used drugs could have a therapeutic role in oncology.
The Study: Investigating the Molecular Impact of Statins in CRC Cells
The study, titled “Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer,” was published in Oncotarget (Volume 16). Using a combination of lipidomics, transcriptomics, proteomics, and 3D tumor models, the researchers explored how two widely prescribed statins, atorvastatin and simvastatin, affect molecular pathways associated with CRC progression. This integrative, multi-omics strategy enabled tracing statin-induced effects across different layers of cellular function, linking lipid, transcript, and protein changes to pathway-level shifts.
Full blog - https://www.oncotarget.org/2025/12/03/repurposing-statins-exploring-anti-tumor-effects-in-colorectal-cancer/
Paper DOI - https://doi.org/10.18632/oncotarget.28755
Correspondence to - Sanjeev Galande - sanjeev.galande@snu.edu.in
Abstract video - https://www.youtube.com/watch?v=A95ICULaH3Y
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Keywords - cancer, colorectal cancer, statins, SATB1, Wnt/β-catenin signaling, tumor-suppressive phenotype
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