MOLECULAR MECHANISM AND THERAPEUTIC POTENTIAL OF BERBERINE, BAICALEIN, ORIDONIN IN THE TREATMENT OF COLORECTAL CANCER – A REVIEW
DOI:
https://doi.org/10.22159/ajpcr.2025v18i4.54115Keywords:
Colorectal cancer, Molecular pathway, Berberine, Baicalein,, Oridonin.Abstract
The aim of this research is to assess the effect of berberine and baicalein and oridonin (ORI) treatment on colorectal cancer (CRC) cells. The research examines how these compounds bring about cellular alterations, stop the cell cycle progression, and trigger cell death. The cancer-fighting agents berberine and baicalein together with ORI demonstrate strong anticancer properties against CRC tissues through metabolic instability and cell cycle arrest leading to apoptosis. ORI affects the activation of TP53/TCF4 mechanisms which creates endoplasmic reticulum stress and then leads to higher reactive oxygen species production alongside calcium ion imbalances. The retinoid X receptor alpha activation mechanism performs better than berberine in colon cancer cell growth inhibition. Berberine suppresses CRC progression through its ability to influence the transforming growth factor-beta signaling pathway together with its inhibitory action on epithelial-mesenchymal transition and its weakening effect on colorectal liver metastasis. The altered composition of gut microbes reduces tissue tumorigenesis as well as total microbial abundance. Berberine shows its anti-metastatic capabilities by blocking the actions of matrix metallopeptidase (MMP)-2 and MMP-9 enzymes which play important roles in cancer cells spreading during metastasis. The suppression of CRC cell growth occurs through berberine-mediated G2/M cell cycle arrest and cell death mechanism that results in cyclin B1 and cdc2 and cdc25c protein downregulation. The anticancer and anti-inflammatory agent baicalein acts as a major element in developing tumorous lesions associated with colitis. The compound speeds up G2/M phase cell cycle arrest through its role in regulating the toll-like receptor 4/nuclear factor-kappa B signaling pathway in HT-29 colon cancer cells. The regulatory mechanisms of this process decrease tumorigenesis that stems from inflammation while also restricting CRC cell multiplication.
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