Curcumin Regulates <scp>VSMC</scp> Phenotype Transition via Modulation of <scp>N</scp>otch and <scp>W</scp>nt Signaling Pathways

Chen, Jing; Xu, Lin; Hu, Xiaorong; Zhang, Jing; Xu, Changwu; Li, Guoqing; Jiang, Hong

doi:10.1002/ddr.21075

Cited by 3 publications

(3 citation statements)

References 27 publications

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“…[19][20][21] Moreover, it has been reported that β-catenin has been considered as a potential therapeutic target for cancer therapy. 11,22 Downregulation of β-catenin expression by small interfering RNA (siRNA) inhibited the progression of various cancers. In this study, we accurately detected the expression level of β-catenin in BC tissues, and the results showed that both the protein and mRNA levels of β-catenin were upregulated in the clinical tissues of BC.…”

Section: Discussionmentioning

confidence: 99%

Curcumin inhibits bladder cancer progression via regulation of β-catenin expression

et al. 2017

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Bladder cancer has a considerable morbidity and mortality impact with particularly poor prognosis. Curcumin has been recently noticed as a polyphenolic compound separated from turmeric to regulate tumor progression. However, the precise molecular mechanism by which curcumin inhibits the invasion and metastasis of bladder cancer cells is not fully elucidated. In this study, we investigate the effect of curcumin on the bladder cancer as well as possible mechanisms of curcumin. The expression of β-catenin was detected by quantitative real-time polymerase chain reaction and immunohistochemical analysis in a series of bladder cancer tissues. In addition, bladder cancer cell lines T24 and 5637 cells were treated with different concentrations of curcumin. The cytotoxic effect of curcumin on cell proliferation of T24 and 5637 cells was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The migration and invasion capacity of T24 and 5637 cells were measured by transwell assay. The effects of curcumin on expression levels of β-catenin and epithelial-mesenchymal transition marker were determined by western blotting. The β-catenin expression was significantly upregulated in bladder cancer tissues when compared with corresponding peri-tumor tissues. Furthermore, curcumin inhibited the cell proliferation of T24 and 5637 cells, and curcumin reduced the migration and invasive ability of T24 and 5637 cells via regulating β-catenin expression and reversing epithelial-mesenchymal transition. Curcumin may be a new drug for bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Curcumin inhibits bladder cancer progression via regulation of β-catenin expression

et al. 2017

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“…In VSMCs, emerging evidences have demonstrated that curcumin could inhibit migration and proliferation. A dose-dependent inhibition (curcumin 5-20 μM) of migration was observed in primary VSMCs, isolated from the aorta of Sprague-Dawley rats [63]. In another study, Li et al [64] found that curcumin could significantly inhibit the proliferation of rat VSMCs by elevating peroxisome proliferator-activated receptor-γ (PPAR-γ) and reducing oxidative stress.…”

Section: Investigations Into Clinicalmentioning

confidence: 98%

Efficacy of Curcumin on Aortic Atherosclerosis: A Systematic Review and Meta-Analysis in Mouse Studies and Insights into Possible Mechanisms

Lin

Chen

et al. 2020

Oxidative Medicine and Cellular Longevity

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Since the first report in 2005, accumulating interests have been focused on the effect of curcumin in atherosclerosis with discrepancies. Therefore, we conducted a systematic review and meta-analysis to comprehensively estimate its effect against atherosclerosis. Literature search was performed on the database of PubMed, EMBASE, and Cochrane Library to identify relevant studies which estimated the effect of curcumin in atherosclerosis. Reporting effects on aortic lesion area was the primary outcome while effects on serum lipid profiles and circulating inflammatory markers were the secondary outcome. A total of 10 studies including 14 independent pairwise experiments were included in our analysis. We clarified that curcumin could significantly reduce aortic atherosclerotic lesion area (SMD=‐0.89, 95% CI: -1.36 to -0.41, P=0.0003), decrease serum lipid profiles (Tc, MD=‐1.005, 95% CI: -1.885 to -0.124, P=0.025; TG, MD=‐0.045, 95% CI: -0.088 to -0.002, P=0.042; LDL-c, MD=‐0.523, 95% CI: -0.896 to -0.149, P=0.006) as well as plasma inflammatory indicators (TNF-α, MD=‐56.641, 95% CI: -86.848 to -26.433, P<0.001; IL-1β, MD=‐5.089, 95% CI: -8.559 to -1.619, P=0.004). Dose-response meta-analysis predicted effective dosage of curcumin between 0 and 347 mg/kg BW per day, which was safe and nontoxic according to the existing publications. The underlying mechanisms were also discussed and might be associated with the modulation of lipid transport and inflammation in cells within artery walls as well as indirect modulations in other tissues. Clinical evidence from nonatherosclerosis populations revealed that curcumin would lower the lipid profiles and inflammatory responses as it has in a mouse model. However, standard preclinical animal trial designs are still needed; further studies focusing on the optimal dose of curcumin against atherosclerosis and RCTs directly in atherosclerosis patients are also warranted.

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“…The β-catenin is the hub of the molecule in the Wnt signaling pathway, which mediates the membrane and facilitates the transfer of molecules from the cytoplasm into the nucleus in the Wnt pathway ( 25 , 26 ). Curcumin also reduced the level of β-catenin gene expression significantly; thus, it has anti-tumor effects through the inhibition of the Wnt signaling pathway ( 18 , 27 , 28 ). Therefore, the mechanism of action of curcumin with regard to tumor inhibition remains to be determined.…”

Section: Introductionmentioning

confidence: 99%

Curcumin inhibits tumor epithelial-mesenchymal transition by downregulating the Wnt signaling pathway and upregulating NKD2 expression in colon cancer cells

Zhang

Chen

et al. 2016

Oncology Reports

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Tumor invasion and metastasis are closely associated with epithelial-mesenchymal transition (EMT). EMT refers to epithelial cells under physiological and pathological conditions that are specific to mesenchymal transition. Curcumin inhibits EMT progression via Wnt signaling. The Wnt signaling pathway is a conservative EMT-related signaling pathway that is involved in the development of various tumors. In the present study, MTS assays were employed to analyze the proliferation of curcumin-treated cells. Naked cuticle homolog 2 (NKD2), chemokine receptor 4 (CXCR4) and antibodies associated with EMT were examined in SW620 colorectal cancer cell lines using western blot analysis and real-time qPCR. NKD2 small-interfering RNA (siRNA) and CXCR4 expression plasmid was synthesized and transfected into the colorectal cancer cell lines, and NKD2 and CXCR4 expression levels were detected. The results showed that curcumin significantly inhibited the proliferation of colorectal cancer cells and upregulated the expression of NKD2 in SW620 colorectal cancer cells and in the xenograft, resulting in the downregulation of key markers in the Wnt signaling. In addition, the progression of ETM was inhibited due to the overexpression of E-cadherin as well as the downregulation of vimentin. Curcumin also inhibited tumor metastasis by downregulating the expression of CXCR4 significantly. The results suggested involvement of the NKD2-Wnt-CXCR4 signaling pathway in colorectal cancer cells. In addition, curcumin is inhibit this signaling and the development of colorectal cancer.

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Curcumin Regulates VSMC Phenotype Transition via Modulation of Notch and Wnt Signaling Pathways

Cited by 3 publications

References 27 publications

Curcumin inhibits bladder cancer progression via regulation of β-catenin expression

Curcumin inhibits bladder cancer progression via regulation of β-catenin expression

Efficacy of Curcumin on Aortic Atherosclerosis: A Systematic Review and Meta-Analysis in Mouse Studies and Insights into Possible Mechanisms

Curcumin inhibits tumor epithelial-mesenchymal transition by downregulating the Wnt signaling pathway and upregulating NKD2 expression in colon cancer cells

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