Baicalin inhibits PDGF-BB-stimulated vascular smooth muscle cell proliferation through suppressing PDGFRβ-ERK signaling and increase in p27 accumulation and prevents injury-induced neointimal hyperplasia

Dong, Lihua; Wen, Jin‐Kun; Miao, Sui-Bing; Jia, Zhenhua; Hu, Haijuan; Sun, Ruoyan; Wu, Yiling; Han, Mei

doi:10.1038/cr.2010.111

Cited by 91 publications

(71 citation statements)

References 33 publications

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“…Baicalin downregulates proto-oncogenes c-jun and c-fos as well as down-regulation of miR-294 expression in mESCs while overexpression of miR-294 in mESCs reverses the alterations in the mESC proliferation and the expression of c-jun and c-fos induced by baicalin. Our results are in good agreement with the observations in cancer cells and vascular smooth muscle cells (VSMCs) [74,75] . Since recent reports have implicated miRNAs in the regulation of proliferation, differentiation and apoptosis in cancer cells and ESCs, it seems possible that miRNAs might also contribute to the cellular mechanisms of decreased proliferation and differentiation and increased apoptosis induced by baicalin in cancer cells.…”

Section: Baicalinsupporting

confidence: 82%

Modulation of miRNAs by Natural Agents: Nature’s way of dealing with cancer

Masika

Zhao

Hescheler

et al. 2015

RNA Dis

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Accumulating lines of evidence have revealed that microRNAs (miRNAs) play critical roles in many biological processes, such as carcinogenesis, angiogenesis, programmed cell death, cell proliferation, invasion, migration, and differentiation. They act either as tumor suppressors or oncogenes, and alteration in their expression patterns has been linked to onset, progression and chemoresistance of various cancers. Moreover, miRNAs are also crucial for the regulation of cancer stem cells (CSCs) self-renewal and proliferation as well as control of Epithelial-to-Mesenchymal Transition (EMT) of cancer cells. Therefore, exploitation of miRNAs as targets for cancer prevention and therapy could be a promising approach. Several experimental and epidemiologic studies have shown that dietary intake of natural agents such as baicalin, ginsenoside, curcumin, resveratrol, genistein, epigallocatechin-3-gallate (EGCG), indole-3-carbinol, 3,3΄-diindolylmethane (DIM) including antioxidants among others is inversely associated with the risk for cancer, demonstrating the inhibitory effects of natural agents on carcinogenesis. Additionally, the anticancer agents from natural agents have been found to inhibit the development and progression of cancer through the regulation of various cancer processes such as apoptosis, cell cycle regulation, differentiation, inflammation, angiogenesis, and metastasis. Importantly, natural agents could significantly impact the expression of tumor-suppressor and oncogenic miRNAs, regulate cellular signaling networks, inhibit cancer cell growth and cancer stem cell self-renewal. This is important for the normalization of altered cellular signaling mechanisms in cancer cells. This postulates a much broader use of natural agents in the prevention and/or treatment of various cancers in combination with conventional chemotherapeutics. However, more in vitro mechanistic experiments, in vivo animal studies, and clinical trials are warranted to realize the true value of natural agents in the prevention and/or treatment of cancer. Herein, we provide an overview of natural agents' modulation of miRNA expression as well as highlight the significance of these observations as potential new strategies in cancer therapies. This review will help us to understand how miRNAs are regulated by natural agents and also help in the development of effective and secure natural agents for therapeutic purposes.

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Section: Baicalinsupporting

confidence: 82%

Modulation of miRNAs by Natural Agents: Nature’s way of dealing with cancer

Masika

Zhao

Hescheler

et al. 2015

RNA Dis

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“…Therefore, tumor growth and metastasis are dependent on angiogenesis and lymphangiogenesis (14)(15)(16). Recently, several studies found that baicalein inhibited proliferation of smooth muscle cells and inhibited LPS-induced angiogenesis in vascular endothelial cells (6,17). Baicalein was also found to inhibit endothelial cell proliferation by inhibiting VEGFR-2 phosphorylation and to decrease the activity of MMP-2 in endothelial cells (18,19).…”

Section: Introductionmentioning

confidence: 99%

“…Baicalein was found to inhibit the proliferation of vascular smooth muscle cells (VSMCs) in cardiovascular disease (24). notably, baicalein inhibited the expression of VEGF and FGFR-2, leading to anticancer effects in lung cancer (20).…”

Section: Cell Proliferationmentioning

confidence: 99%

Baicalein inhibits tumor progression by inhibiting tumor cell growth and tumor angiogenesis

et al. 2017

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Abstract. Baicalein, a herbal medicine, is a natural flavonoid isolated from the roots of Scutellaria baicalensis Georgi. It is known for its anticancer, anti-inflammatory and neuroprotective properties. Despite these well-known properties, it is not yet clear what effect baicalein has on tumor progression. Therefore, in the present study, we used B16F10 cells, Lewis lung carcinoma (LLC) cells, and human umbilical vein endothelial cells (HUVECs) to investigate the effect of baicalein on cell proliferation and viability, migration and tube formation in vitro. In addition, an experimental animal model was used to observe the growth rate and metastasis of tumors and tumor vessel formation in vivo. Our results showed that baicalein decreased the proliferation and migration and induced tumor cell death via caspase-3 activation in the B16F10 and LLC cells, and strongly inhibited tube formation and cell migration in HUVECs. Furthermore, mouse models showed that baicalein reduced the tumor volume and greatly reduced the tumor growth rate in the early stages of tumor progression, and the baicalein-treated groups had significantly reduced expression of CD31 (endothelial cell marker) and α-SMA (mural cell marker) in the tumors, indicating that baicalein inhibits tumor angiogenesis by disrupting tumor vasculature development. Comparison of the lymph node and lung samples collected from the baicalein-treated group, and the untreated group showed that baicalein reduced metastasis of the tumor to these tissues. In summary, baicalein reduced tumor progression and metastasis, directly induced tumor cell death, and inhibited tumor angiogenesis. Our results strongly demonstrate that baicalein is a potential chemotherapeutic agent.

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“…Kip1 is regulated by multiple signaling pathways, including the Ras/MAPK/ERK1/2 [33][34][35] and PI3K/Akt/mTOR pathways. 36,37 These observations prompted us to examine the impact of rapamycin on The levels of p-p70S6K and p70S6K were analyzed by Western blotting.…”

Section: Discussionmentioning

confidence: 99%

Rapamycin ameliorates IgA nephropathy via cell cycle-dependent mechanisms

Tian

Wang

et al. 2014

Exp Biol Med (Maywood)

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IgA nephropathy is the most frequent type of glomerulonephritis worldwide. The role of cell cycle regulation in the pathogenesis of IgA nephropathy has been studied. The present study was designed to explore whether rapamycin ameliorates IgA nephropathy via cell cycle-dependent mechanisms. After establishing an IgA nephropathy model, rats were randomly divided into four groups. Coomassie Brilliant Blue was used to measure the 24-h urinary protein levels. Renal function was determined using an autoanalyzer. Proliferation was assayed via Proliferating Cell Nuclear Antigen (PCNA) immunohistochemistry. Rat mesangial cells were cultured and divided into the six groups. Methylthiazolyldiphenyl-tetrazolium bromide (MTT) and flow cytometry were used to detect cell proliferation and the cell cycle phase. Western blotting was performed to determine cyclin E, cyclin-dependent kinase 2, p27Kip1 , p70S6K/p-p70S6K, and extracellular signal-regulated kinase 1/2/p-extracellular signal-regulated kinase 1/2 protein expression. A low dose of the mammalian target of rapamycin (mTOR) inhibitor rapamycin prevented an additional increase in proteinuria, protected kidney function, and reduced IgA deposition in a model of IgA nephropathy. Rapamycin inhibited mesangial cell proliferation and arrested the cell cycle in the G1 phase. Rapamycin did not affect the expression of cyclin E and cyclindependent kinase 2. However, rapamycin upregulated p27 Kip1 at least in part via AKT (also known as protein kinase B)/mTOR. In conclusion, rapamycin can affect cell cycle regulation to inhibit mesangial cell proliferation, thereby reduce IgA deposition, and slow the progression of IgAN.

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Baicalin inhibits PDGF-BB-stimulated vascular smooth muscle cell proliferation through suppressing PDGFRβ-ERK signaling and increase in p27 accumulation and prevents injury-induced neointimal hyperplasia

Cited by 91 publications

References 33 publications

Modulation of miRNAs by Natural Agents: Nature’s way of dealing with cancer

Modulation of miRNAs by Natural Agents: Nature’s way of dealing with cancer

Baicalein inhibits tumor progression by inhibiting tumor cell growth and tumor angiogenesis

Rapamycin ameliorates IgA nephropathy via cell cycle-dependent mechanisms

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