Berberine Inhibits Pulmonary Metastasis through Down‐regulation of MMP in Metastatic B16F‐10 Melanoma Cells

Purayil, Hamsa Thayele; Kuttan, Girija

doi:10.1002/ptr.3586

Cited by 40 publications

(29 citation statements)

References 44 publications

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“…BBR inhibits melanoma cell invasion and metastasis by inhibition of COX-2, PGE2 and PGE2 receptors [17] and several other signaling molecules such as ERK1/2, NF-κB, ATF-2 and CREB which are involved in the transcriptional regulation of matrix metalloproteinase (MMP) gene expression [30]. Berberine also exerted anti-invasive effect on HepG2 cells through suppression of MMP-9 expression [12].…”

Section: Discussionmentioning

confidence: 99%

Epithelial-to-mesenchymal transition markers to predict response of Berberine in suppressing lung cancer invasion and metastasis

Xin²,

et al. 2014

J Transl Med

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BackgroundThe effects of berberine on the metastatic potential of lung cancer cells and its underlying mechanisms have not been fully elucidated. Since epithelial-to-mesenchymal transition is a cellular process associated with cancer invasion and metastasis, we attempted to investigate the potential use of berberine as an inhibitor of TGF-β1-induced epithelial-to-mesenchymal in A549 cells.MethodsIn this study, we investigated the anticancer activity of berberine against A549 cells in vitro and in vivo. BBR-induced apoptosis of the human lung cancer cells was determined by flow cytometry. The ability of BBR to inhibit TGF-β-induced EMT was examined by QRT-PCR and Western blotting. The impact of BBR on A549 cell migration and invasion was evaluated by transwell assay.ResultsWe demonstrated that TGF-β1 induced epithelial-to-mesenchymal to promote lung cancer invasion and metastasis. Berberine inhibited invasion and migration of A549 cells, increased expression of the epithelial phenotype marker E-cadherin, repressed the expression of the mesenchymal phenotype marker Vimentin, as well as decreased the level of epithelial-to-mesenchymal -inducing transcription factors Snail1 and Slug during the initiation of TGF-β1-induced epithelial-to-mesenchymal. Furthermore, berberine inhibited growth of lung cancer cells in vivo xenograft.ConclusionsOur findings provided new evidence that berberine is an effective inhibitor of the metastatic potential of A549 cells through suppression of TGF-β1-induced epithelial-to-mesenchymal.

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Section: Discussionmentioning

confidence: 99%

Epithelial-to-mesenchymal transition markers to predict response of Berberine in suppressing lung cancer invasion and metastasis

Xin²,

et al. 2014

J Transl Med

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“…Interestingly, these effects might be specific for cancer cells [12]. The effect of berberine on invasion, migration, metastasis, and angiogenesis is mediated through the inhibition of focal adhesion kinase (FAK), NF- κ B, urokinase-type plasminogen-activator (u-PA), matrix metalloproteinase 2 (MMP-2), and matrix metalloproteinase 9 (MMP-9) [20, 29]; reduction of Rho kinase-mediated Ezrin phosphorylation [19]; reduction of the expression of COX-2, prostaglandin E, and prostaglandin E receptors [30]; downregulation of hypoxia-inducible factor 1 (HIF-1), vascular endothelial growth factor (VEGF), proinflammatory mediators [21, 22], and so forth. …”

Section: Alkaloids With Anticancer Effects and The Related Mechanmentioning

confidence: 99%

Alkaloids Isolated from Natural Herbs as the Anticancer Agents

Bao

Chen

et al. 2012

Evidence-Based Complementary and Alternative Medicine

296

156

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Alkaloids are important chemical compounds that serve as a rich reservoir for drug discovery. Several alkaloids isolated from natural herbs exhibit antiproliferation and antimetastasis effects on various types of cancers both in vitro and in vivo. Alkaloids, such as camptothecin and vinblastine, have already been successfully developed into anticancer drugs. This paper focuses on the naturally derived alkaloids with prospective anticancer properties, such as berberine, evodiamine, matrine, piperine, sanguinarine, and tetrandrine, and summarizes the mechanisms of action of these compounds. Based on the information in the literature that is summarized in this paper, the use of alkaloids as anticancer agents is very promising, but more research and clinical trials are necessary before final recommendations on specific alkaloids can be made.

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“…Berberine has a long history of being used as a therapeutic agent to treat a variety of diseases, including cancer. It has been reported that BBR by exhibiting multiple pharmacological activities, including anti-inflammatory [8], anti-hypertensive [9], cholesterol-lowering [10], anti-diarrheal [11,12], anti-microbial [13,14] activities, and the anti-tumor effect of BBR was more and more emphasized in the past several decades [15,16]. BBR has been shown to exhibit anti-proliferation effects against cancer cells of different origins, including glioblastoma [17], melanoma [18], colon cancer [19], breast cancer [20,21], prostate cancer [22] and so on.…”

Section: Introductionmentioning

confidence: 99%

Berberine Targets AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF and Cytochrome-c/Caspase Signaling to Suppress Human Cancer Cell Growth

Chen

Guo

et al. 2013

PLoS ONE

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Berberine (BBR), an isoquinoline derivative alkaloid isolated from Chinese herbs, has a long history of uses for the treatment of multiple diseases, including cancers. However, the precise mechanisms of actions of BBR in human lung cancer cells remain unclear. In this study, we investigated the molecular mechanisms by which BBR inhibits cell growth in human non-small-cell lung cancer (NSCLC) cells. Treatment with BBR promoted cell morphology change, inhibited cell migration, proliferation and colony formation, and induced cell apoptosis. Further molecular mechanism study showed that BBR simultaneously targeted multiple cell signaling pathways to inhibit NSCLC cell growth. Treatment with BBR inhibited AP-2α and AP-2β expression and abrogated their binding on hTERT promoters, thereby inhibiting hTERT expression. Knockdown of AP-2α and AP-2β by siRNA considerably augmented the BBR-mediated inhibition of cell growth. BBR also suppressed the nuclear translocation of p50/p65 NF-κB proteins and their binding to COX-2 promoter, causing inhibition of COX-2. BBR also downregulated HIF-1α and VEGF expression and inhibited Akt and ERK phosphorylation. Knockdown of HIF-1α by siRNA considerably augmented the BBR-mediated inhibition of cell growth. Moreover, BBR treatment triggered cytochrome-c release from mitochondrial inter-membrane space into cytosol, promoted cleavage of caspase and PARP, and affected expression of BAX and Bcl-2, thereby activating apoptotic pathway. Taken together, these results demonstrated that BBR inhibited NSCLC cell growth by simultaneously targeting AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF, PI3K/AKT, Raf/MEK/ERK and cytochrome-c/caspase signaling pathways. Our findings provide new insights into understanding the anticancer mechanisms of BBR in human lung cancer therapy.

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Berberine Inhibits Pulmonary Metastasis through Down‐regulation of MMP in Metastatic B16F‐10 Melanoma Cells

Cited by 40 publications

References 44 publications

Epithelial-to-mesenchymal transition markers to predict response of Berberine in suppressing lung cancer invasion and metastasis

Epithelial-to-mesenchymal transition markers to predict response of Berberine in suppressing lung cancer invasion and metastasis

Alkaloids Isolated from Natural Herbs as the Anticancer Agents

Berberine Targets AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF and Cytochrome-c/Caspase Signaling to Suppress Human Cancer Cell Growth

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