Berberine suppressed epithelial mesenchymal transition through cross-talk regulation of PI3K/AKT and RARα/RARβ in melanoma cells

Kou, Yu; Li, Lei; Li, Hong; Tan, Yu‐Hui; Li, Bin; Wang, Kun; Du, Baoheng

doi:10.1016/j.bbrc.2016.09.061

Cited by 60 publications

(48 citation statements)

References 28 publications

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“…The low expression of PTEN results in its disability to effectively inhibit the abnormal activation of the PDK/Akt pathway, and thus leads to tumor migration, which is associated with the highest occurrence rate in prostate, endometrial cancer, glioma and MM (10). As is reported, PTEN gene changes can be seen in 30–50% of MM cell lines and 5–20% of MM cells (9,11). The activated PI3K/Akt may further activate its downstream molecule mTOR through the TSC1/2 complex, and the activated mTOR can activate its two downstream molecules subsequently, which are the translation inhibitory molecule eIF-4E binding protein 1 (4E-BP1) and ribosomal protein p70S6K (10,12).…”

Section: Introductionsupporting

confidence: 65%

“…PTEN can dephosphorylate phosphatidylinositol 3,4,5-trisphosphate (PIP3), and thus, weaken the PI3K-derived activation signal and indirectly inhibit the activation of Akt (9). The low expression of PTEN results in its disability to effectively inhibit the abnormal activation of the PDK/Akt pathway, and thus leads to tumor migration, which is associated with the highest occurrence rate in prostate, endometrial cancer, glioma and MM (10).…”

Section: Introductionmentioning

confidence: 99%

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Circulating microRNA-194 regulates human melanoma cells via PI3K/AKT/FoxO3a and p53/p21 signaling pathway

et al. 2017

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In the present study, we analyzed the role of microRNA-194 circulating regulated human melanoma cell growth. We found that microRNA-194 expression was markedly suppressed in human melanoma patients, compared with negative control group. Next, disease-free survival (DFS) and overall survival (OS) of high expression in human melanoma patients was higher than those of low expression in human melanoma patients. MicroRNA-194 overexpression inhibited cell proliferation, induced apoptosis, increased caspase-3/−9 activities and promoted Bax/Bcl-2 of human melanoma cells. Furthermore, microRNA-194 overexpression also suppressed PI3K/AKT/FoxO3a signaling pathway and induced p53/p21 signaling pathway. PI3K inhibitor, suppressed PI3K, phosphorylation-AKT, FoxO3a protein expression and increased the effects of microRNA-194 overexpression on cell growth, apoptosis, caspase-3/−9 activities and Bax/Bcl-2 protein expression of human melanoma cells through the induction of p53/p21 signaling pathway. Taken together, these data indicate that circulating microRNA-194 regulated human melanoma cells via PI3K/AKT/FoxO3a and p53/p21 signaling pathway.

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Section: Introductionsupporting

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Circulating microRNA-194 regulates human melanoma cells via PI3K/AKT/FoxO3a and p53/p21 signaling pathway

et al. 2017

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“…Today, N‐cadherin is regarded as a vital marker of EMT . Neoexpression or upregulated expression of N‐cadherin has been reported to accelerate migration and invasion of cancer cells, which showed a contrary function to those of E‐cadherin . This process of reciprocally downregulating E‐cadherin and upregulating N‐cadherin is known as cadherin switching that characterizes EMT .…”

Section: Introductionmentioning

confidence: 99%

“…Some studies indicate that N‐cadherin boosts the combination of fibroblast growth factor (FGF) with the receptor to initiate FGFR signal transduction, thereby inducing signalling cascades that promote migration and invasion of cancer cells . Furthermore, studies have shown that N‐cadherin promotes cells survival and protects cancer cells from apoptosis by activating the phosphatidylinositol 3‐kinase (PI3K)‐AKT (also known as protein kinase B) pathway . Therefore, N‐cadherin presents distinct functions from its adhesion activity.…”

Section: Introductionmentioning

confidence: 99%

Upregulated N‐cadherin expression is associated with poor prognosis in epithelial‐derived solid tumours: A meta‐analysis

Luo

Zhang

et al. 2018

Eur J Clin Investigation

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BackgroundN‐cadherin is an important molecular in epithelial‐mesenchymal transition (EMT) and has been reported to be associated with aggressive behaviours of tumours. However, prognostic value of N‐cadherin in solid malignancies remains controversially.Materials and MethodsThe Pubmed/MELINE and EMBASE databases were used for a comprehensive literature searching. Pooled risk ratio (RR) and hazard ratio (HR) with their corresponding 95% confidence intervals (CIs) were employed to quantify the prognostic role.ResultsInvolving 36 studies with 5705 patients were performed to investigate relationships between N‐cadherin upregulation and clinicopathological features, survival. Results suggested upregulated N‐cadherin was associated with lymph node metastasis (RR = 1.16, 95% CI [1.00, 1.35]), higher histological grade (RR = 1.36, 95%CI [1.14, 1.62]), angiolymphatic invasion (RR = 1.19, 95% CI [1.06, 1.34]) and advanced clinical stage (RR = 1.32, 95% CI [1.06, 1.64]), while upregulated N‐cadherin was apt to be associated with distant metastasis (RR = 1.43, 95% CI [0.99, 2.05]). Moreover, N‐cadherin was correlated with poor prognosis of 3‐year survival (HR = 1.78, 95% CI [1.51, 2.10]), 5‐year survival (HR = 1.57, 95% CI [1.17, 2.10]) and overall survival (OS) (HR = 1.32, 95% CI [1.20, 1.44]). Subgroup analyses according to cancer types were also conducted for applying these conclusions to some tumours more properly. No publication bias was found except subgroup analysis of distant metastasis (P = .652 for Begg's test and 0.023 for Egger's test).ConclusionsTaken together, upregulation of N‐cadherin is associated with more aggressive behaviours of epithelial‐derived solid malignancies and can be regarded as a predictor of poor survival.

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“…In contrast, RARbeta and RARgamma signaling were upregulated. BBR treatment may reverse EMT in melanoma cells [279]. …”

Section: Introductionmentioning

confidence: 99%

Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs

McCubrey¹,

Lertpiriyapong²,

Steelman³

et al. 2017

aging

195

128

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Natural products or nutraceuticals have been shown to elicit anti-aging, anti-cancer and other health-enhancing effects. A key target of the effects of natural products may be the regulation of microRNA (miR) expression which results in cell death or prevents aging, diabetes, cardiovascular and other diseases. This review will focus on a few natural products, especially on resveratrol (RES), curcumin (CUR) and berberine (BBR). RES is obtained from the skins of grapes and other fruits and berries. RES may extend human lifespan by activating the sirtuins and SIRT1 molecules. CUR is isolated from the root of turmeric (Curcuma longa). CUR is currently used in the treatment of many disorders, especially in those involving an inflammatory process. CUR and modified derivatives have been shown to have potent anti-cancer effects, especially on cancer stem cells (CSC). BBR is also isolated from various plants (e.g., Coptis chinensis) and has been used for centuries in traditional medicine to treat diseases such as adult- onset diabetes. Understanding the benefits of these and other nutraceuticals may result in approaches to improve human health.

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Berberine suppressed epithelial mesenchymal transition through cross-talk regulation of PI3K/AKT and RARα/RARβ in melanoma cells

Cited by 60 publications

References 28 publications

Circulating microRNA-194 regulates human melanoma cells via PI3K/AKT/FoxO3a and p53/p21 signaling pathway

Circulating microRNA-194 regulates human melanoma cells via PI3K/AKT/FoxO3a and p53/p21 signaling pathway

Upregulated N‐cadherin expression is associated with poor prognosis in epithelial‐derived solid tumours: A meta‐analysis

Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs

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