Effect of berberine on proliferation, cell cycle and apoptosis in HeLa and L1210 cells

Jantová, Soňa; Čipák, Luboš; Cernáková, M; Kostálová, D

doi:10.1211/002235703322277186

Cited by 153 publications

(77 citation statements)

References 33 publications

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“…In the present study, 10-20 µM of berberine significantly induced G1 arrest in CCA cells in dose and time dependent fashions. The induction of cell cycle arrest at G1 phase by low doses of berberine (<50 µM) were demonstrated in several cancer cell lines including human bladder cancer cells, 22) a murine leukemia cell line 23) and a non-Ov-associated CCA cell line. 15) In addition, high doses of berberine (>50 µM) promoted G2/M arrest or induction of apoptosis as reported in many human cancer cells, e.g., gastric cancer 24) and prostate cancer.…”

Section: )mentioning

confidence: 99%

Berberine Induces Cell Cycle Arrest in Cholangiocarcinoma Cell Lines <i>via</i> Inhibition of NF-κB and STAT3 Pathways

Puthdee

Seubwai

Vaeteewoottacharn

et al. 2017

Biological & Pharmaceutical Bulletin

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Berberine is a natural compound found in several herbs. Anticancer activity of berberine was reported in several cancers, however, little is known regarding the effects of berberine against cholangiocarcinoma (CCA). In this study, the growth inhibitory effects of berberine on CCA cell lines and its molecular mechanisms were explored. Cell growth and cell cycle distribution were examined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. The expression levels of cell cycle regulatory proteins were determined by Western blot analysis. Berberine significantly inhibited growth of CCA cell lines in a dose and time dependent fashion. The inhibition was largely attributed to cell cycle arrest at the G1 phase through the reduction of cyclin D1, and cyclin E. Moreover, berberine could reduce the expression and activation of signal transducers and activator of transcription 3 (STAT3) and probably nuclear factor-kappaB (NF-κB) via suppression of extracellular signal-regulated kinase (ERK) 1/2 action. These results highlight the potential of berberine to be a multi-target agent for CCA treatment.

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Section: )mentioning

confidence: 99%

Berberine Induces Cell Cycle Arrest in Cholangiocarcinoma Cell Lines <i>via</i> Inhibition of NF-κB and STAT3 Pathways

Puthdee

Seubwai

Vaeteewoottacharn

et al. 2017

Biological & Pharmaceutical Bulletin

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“…Berberine has been reported to induce apoptosis through a mitochondrial pathway that includes upregulation of p53, alterations in Bcl-2/Bax ratios, a decrease in mitochondrial membrane potential, release of cytochrome c, and activation of caspases [2,[6][7][8][9][10][11][12]. This is of particular interest in light of studies demonstrating a mitochondrial localization of berberine, raising the possibility that apoptosis results from mitochondrial damage induced by berberine.…”

Section: Introductionmentioning

confidence: 99%

Different concentrations of berberine result in distinct cellular localization patterns and cell cycle effects in a melanoma cell line

Serafim

Oliveira

Sardão

et al. 2007

Cancer Chemother Pharmacol

118

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Purpose Natural products represent a rich reservoir of potential small molecule inhibitors exhibiting antiproliferative and tumoricidal properties. An example is the isoquinoline alkaloid berberine, which is found in plants such as goldenseal (Hydrastis canadensis). Studies have shown that berberine is able to trigger apoptosis in diVerent malignant cell lines, and can also lead to cell cycle arrest at sub-apoptotic doses. A particularly interesting feature of berberine is the fact that it is a Xuorescent molecule, and its uptake and distribution in cells can be studied by Xow cytometry and epiXuorescence microscopy. To test the relationships between berberine uptake, distribution and cellular eVect in melanoma cells, K1735-M2 mouse and WM793 human melanoma cells were treated with diVerent concentrations of berberine, and alterations in cell cycle progression, DNA synthesis, cell proliferation, and cell death measured. Methods Cell proliferation was measured by sulforhodamine B assays, cell death by Xow cytometry, berberine uptake and distribution by laser scanning confocal microscopy and Xow cytometry, cell cycle progression by Xow cytometry, and DNA synthesis, M-phase, and mitochondrial eVects by immunolabeling and epiXuorescence microscopy methods. Results In these melanoma cell lines, berberine at low doses (12.5-50 M) is concentrated in mitochondria and promotes G1 arrest. In contrast, higher doses (over 50 M) result in cytoplasmic and nuclear berberine accumulation, and G2 arrest. DNA synthesis is not markedly aVected by low doses of berberine, but 100 M is strongly inhibitory. Even at 100 M, berberine inhibits cell growth with relatively little induction of apoptosis. Conclusion Berberine displays multiphasic eVects in these malignant cell lines, which are correlated with the concentration and intracellular distribution of this alkaloid. These results help explain some of the conXicting information in the literature regarding the eVects of berberine, and suggest that its use in clinical development may be more as a cytostatic agent than a cytotoxic compound.

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“…A report from Ko et al demonstrated that berberine has vasorelaxant and anti-proliferative effects on vascular SMCs [21]. In addition, Jantova et al had disclosed that berberine could cause G1/0 arrest in cancer cell lines [22]. Recently, Lee et al reported that berberine could inhibit SMC growth and inhibit Akt activation after angiotensin II stimulation [23].…”

Section: Introductionmentioning

confidence: 99%

Berberine suppresses MEK/ERK-dependent Egr-1 signaling pathway and inhibits vascular smooth muscle cell regrowth after in vitro mechanical injury

Liang

Ting

Yin

et al. 2006

Biochemical Pharmacology

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Vascular smooth muscle cell (SMC) proliferation plays an important role in the pathogenesis of atherosclerosis and post-angioplasty restenosis. Berberine is a well-known component of the Chinese herb medicine Huanglian (Coptis chinensis), and is capable of inhibiting SMC contraction and proliferation, yet the exact mechanism is unknown. We therefore investigated the effect of berberine on SMC growth after mechanic injury in vitro. DNA synthesis and cell proliferation assay were performed to show that berberine inhibited serum-stimulated rat aortic SMC growth in a concentration-dependent manner. Mechanical injury with sterile pipette tip stimulated the regrowth of SMCs. Treatment with berberine prevented the regrowth and migration of SMCs into the denuded trauma zone. Western blot analysis showed that activation of the MEK1/2 (mitogen-activated protein kinase kinase 1/2), extracellular signal-regulated kinase (ERK), and up-regulation of early growth response gene (Egr-1), c-Fos and Cyclin D1 were observed sequentially after mechanic injury in vitro. Semi-quantitative reverse-transcription PCR assay further confirmed the increase of Egr-1, cFos, platelet-derived growth factor (PDGF) and Cyclin D1 expression in a transcriptional level. However, berberine significantly attenuated MEK/ERK activation and downstream target (Egr-1, cFos, Cyclin D1 and PDGF-A) expression after mechanic injury in vitro. Our study showed that berberine blocked injury-induced SMC regrowth by inactivation of ERK/Egr-1 signaling pathway thereby preventing early signaling induced by injury in vitro. The anti-proliferative properties of berberine may be useful in treating disorders due to inappropriate SMC growth.

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Effect of berberine on proliferation, cell cycle and apoptosis in HeLa and L1210 cells

Cited by 153 publications

References 33 publications

Berberine Induces Cell Cycle Arrest in Cholangiocarcinoma Cell Lines <i>via</i> Inhibition of NF-κB and STAT3 Pathways

Berberine Induces Cell Cycle Arrest in Cholangiocarcinoma Cell Lines <i>via</i> Inhibition of NF-κB and STAT3 Pathways

Different concentrations of berberine result in distinct cellular localization patterns and cell cycle effects in a melanoma cell line

Berberine suppresses MEK/ERK-dependent Egr-1 signaling pathway and inhibits vascular smooth muscle cell regrowth after in vitro mechanical injury

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