Cell cycle analysis of Coptidis Rhizoma-treated cancer cells showed the accumulation of cells in the G₀/G₁ phase and relative decrease of the S phase. These results support the possibility that the use of Coptidis Rhizoma containing abundant berberine may be useful as one of alternative therapies for esophageal cancers.

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The enzyme cyclooxygenase-2 (COX-2) is abundantly expressed in colon cancer cells and plays a key role in colon tumorigenesis. Compounds inhibiting COX-2 transcriptional activity have therefore potentially a chemopreventive property against colon tumor formation.

The present findings may further explain the mechanism of anti-inflammatory and anti-tumor promoting effects of berberine.

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Anti - Cancer - Berberine, a compound isolated from medicinal herbs, has been reported with many pharmacological effects related to anti-cancer and anti-inflammation capabilities. In this study, we observed that berberine exerted a dose- and time-dependent inhibitory effect on the motility and invasion ability of a highly metastatic A549 cells under non-cytotoxic concentrations.

These findings suggest that berberine possesses an anti-metastatic effect in non-small lung cancer cell and may, therefore, be helpful in clinical treatment.

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The cell death induced by berberine alone or the combination of berberine and irradiation was suppressed by the anti‐oxidant, N‐acetyl cysteine (NAC). Taken together, the present results clearly indicate that the combination of berberine and gamma‐radiation enhance the anti‐cancer effects through the p38 MAPK pathway and ROS generation.

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Chemically induced carcinogenesis models in the rat are widely used for studying the biology of cancer and for developing and evaluating cancer prevention strategies.

The present study suggests that berberine prevents the appearance of malignant morphology and ultrastructural changes of AOM induced cancer by producing apoptosis like changes. Thus berberine inhibits neoplastic transformation by the induction of antioxidant defence system and ability to induce apoptotic like changes—thus elucidating its anti cancer role.

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Pretreatment of cells with 32 μM berberine for 24 h prior to Paclitaxel treatment resulted in increased viability as compared to that of Paclitaxel-treated cells. In addition, Paclitaxel-induced apoptosis and/or G2/M arrest in these three cancer cell lines. Pretreatment of cells with berberine prior to Paclitaxel blocked the Paclitaxel-induced cell cycle responses and morphological changes.

These results together suggest that berberine modulated the expression and function of pgp-170 that leads to reduced response to Paclitaxel in digestive track cancer cells.

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