ArticleMolecular and cellular biochemistry2026
Carvacrol induces apoptosis, modulates oxidative stress, and promotes G0/G1 cell cycle arrest in colorectal cancer cells.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Colorectal cancer (CRC) remains a major therapeutic challenge due to toxicity, low tumor specificity, and multidrug resistance. Carvacrol, a natural monoterpenoid phenol with notable anticancer, anti-inflammatory, and antioxidant properties, has emerged as a promising compound. This study evaluated the anticancer efficacy and underlying molecular mechanisms of carvacrol in HT-29 CRC cells and CCD-18Co normal colon fibroblasts. Cell viability was assessed using CVDK-8, migration by wound healing assay, and apoptosis, reactive oxygen species (ROS) levels, and cell cycle distribution by flow cytometry. Expression levels of PDHA1, SOX2, CASP3, POLB, ABCC1, and E2F4 were quantified by qPCR. Bioinformatic analyses were performed using GEPIA2 for overall survival (OS) and disease-free survival (DFS) evaluation and STRING for protein-protein interaction (PPI) network analysis. Carvacrol exhibited dose-dependent cytotoxicity in HT-29 cells (IC
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