Berberine Inhibits the Metastatic Ability of Prostate Cancer Cells by Suppressing Epithelial-to-Mesenchymal Transition (EMT)-Associated Genes with Predictive and Prognostic Relevance

Liu, Chia-Hung; Tang, Wanchun; Sia, Peik; Huang, Chi-Chen; Yang, Pei–Ming; Wu, Ming–Heng; Lai, I-Lu; Lee, Kuen-Haur

doi:10.7150/ijms.9982

Cited by 71 publications

(49 citation statements)

References 36 publications

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“…EMT is an important step in the invasion and metastasis of cancer cells, and a physiological and pathological phenomenon, characterised by the loss of epithelial features and the acquisition of intercellular characteristics (Liu et al 2015). In the process of EMT, the expression of E-cadherin, a membrane protein mediating the tight junction between epithelial cells, is downregulated, and the expression of connexin between mesenchymal cells, such as N-cadherin and vimentin, is upregulated .…”

Section: Effect Of Ck Combined With Cisplatin On Fn Levels In the Supmentioning

confidence: 99%

Effects of ginsenoside compound K combined with cisplatin on the proliferation, apoptosis and epithelial mesenchymal transition in MCF-7 cells of human breast cancer

Zhang

2015

Pharmaceutical Biology

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Context: Breast cancer seriously harms the health of women and there are currently few therapeutic options for patients with breast cancer. Objective: Effects of ginsenoside compound K (CK) in combination with cisplatin (DDP) on the proliferation, apoptosis, and epithelial mesenchymal transition (EMT) of MCF-7 cells were studied. Materials and methods: MCF-7 cells were divided into CK (50 mmol/L) group, DDP (10 mg/L) group, CK (50 mmol/L) +DDP (10 mg/L) group, and control (CON) group. The cells in the CON group were not treated with any drugs. Proliferation, apoptosis, expression of E-cadherin, N-cadherin, vimentin, protein kinase B (Akt), phosphorylated Akt (p-Akt), and level of fibronectin (FN) in MCF-7 cells were detected by methyl thiazolyl tetrazolium (MTT), flow cytometry, western blotting, and enzyme-linked immuno sorbent assay (ELISA), respectively. Results: The proliferation inhibition rates in CK, DDP, and CK + DDP groups at 48 h were 19.18 ± 2.25, 21.34 ± 2.84, and 43.37 ± 5.62, respectively. The apoptosis rates were 2.85 ± 0.56, 13.37 ± 2.28,

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Section: Effect Of Ck Combined With Cisplatin On Fn Levels In the Supmentioning

confidence: 99%

Effects of ginsenoside compound K combined with cisplatin on the proliferation, apoptosis and epithelial mesenchymal transition in MCF-7 cells of human breast cancer

Zhang

2015

Pharmaceutical Biology

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“…BBR reverses the phenotypic transition and inhibits the migration of the HCoEpiC cells undergoing EMT through regulation of Smad2 and p-Smad3 in the TGF-β pathway Although a large number of studies have illustrated the antagonistic effect of BBR on EMT in various models (S Kim et al, 2018;Liu et al, 2015),. our knowledge about this effect of BBR on EMT in F I G U R E 1 HCoEpiC cells are treated by SW480-derived CM or induction of SW480 in cultured HCoEpiC cells using two kinds of models and intervention of berberine (BBR).…”

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confidence: 99%

Berberine reversed the epithelial‐mesenchymal transition of normal colonic epithelial cells induced by SW480 cells through regulating the important components in the TGF‐β pathway

Huang

Tao

Wang³

et al. 2018

Journal Cellular Physiology

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Stroma‐tumor interactions within microenvironment play a crucial role in tumor development and growth. Cellular transdifferentiation in the stroma is a prerequisite for tumor formation. Targeting the interactions maybe a promising anticancer strategy. Berberine (BBR) has been confirmed to have anticancer and anti‐inflammatory effects. We found for the first time that colon cancer cells SW480 induced spindle‐like morphological changes and downregulation of E‐cadherin and upregulation of vimentin and alpha‐smooth muscle actin in colon epithelial cells HCoEpiCs by using transwell coculture system and conditioned medium from SW480. The conditioned medium also promoted the migration of HCoEpiCs. This transition was inhibited by a transforming growth factor‐β receptor inhibitor LY364947. BBR (50 and 100 µg/ml) reversed the EMT‐like transition and repressed the migration in HCoEpiCs. Further results demonstrated that downregulation of TβRII, Smad2, p‐Smad3, and overexpression of Smad3 participated in the SW480‐induced phenotypic transition of HCoEpiCs. In addition, BBR upregulated the expressions of TβRII, Smad2, and p‐Smad3. In conclusion, our findings suggest that BBR exerts the anti‐EMT and antimigration effect by mediating the expression of TβRII, Smad2, and p‐Smad3.

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“…The strong anti-tumor growth via induction of cell cycle arrest, apoptosis and inhibition of metastasis have been shown in several in vitro and in vivo studies. [6][7][8] Little, however, is known about the anti-cancer activities of berberine on CCA. The present work was aimed to determine the anti-cancer activities and potential molecular mechanisms of berberine on CCA cell lines.…”

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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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Berberine Inhibits the Metastatic Ability of Prostate Cancer Cells by Suppressing Epithelial-to-Mesenchymal Transition (EMT)-Associated Genes with Predictive and Prognostic Relevance

Cited by 71 publications

References 36 publications

Effects of ginsenoside compound K combined with cisplatin on the proliferation, apoptosis and epithelial mesenchymal transition in MCF-7 cells of human breast cancer

Effects of ginsenoside compound K combined with cisplatin on the proliferation, apoptosis and epithelial mesenchymal transition in MCF-7 cells of human breast cancer

Berberine reversed the epithelial‐mesenchymal transition of normal colonic epithelial cells induced by SW480 cells through regulating the important components in the TGF‐β pathway

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

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