EPO gene expression induces the proliferation, migration and invasion of bladder cancer cells through the p21WAF1-mediated ERK1/2/NF-κB/MMP-9 pathway

Park, Sung Lyea; Won, Se Yeon; Song, Junhui; Kim, Wun-Jae; Moon, Sung‐Kwon

doi:10.3892/or.2014.3428

Cited by 10 publications

(9 citation statements)

References 30 publications

(65 reference statements)

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“…Comparisons were made to unstimulated cells. Ã P < 0.05. cells [Park et al, 2014[Park et al, , 2015. Our findings support our proposal that EPO induces an EMT process in MCF10A cells.…”

Section: Discussionsupporting

confidence: 91%

“…We propose that EPO induces an increase of vimentin and Snail2 expression through a NFκB‐dependent pathway. Supporting our proposal, it has been demonstrated that EPO gene expression induces migration and invasion through MMP‐9 expression and NFκB activation in vascular smooth muscle cells and bladder cancer cells [Park et al, , ]. Our findings support our proposal that EPO induces an EMT process in MCF10A cells.…”

Section: Discussionsupporting

confidence: 91%

“…We propose that EPO induces migration/invasion of epithelial mammary tumor cells. Supporting our proposal, it has been demonstrated that EPO gene expression induces migration of human bladder carcinoma cells [Park et al, ].…”

Section: Discussionsupporting

confidence: 85%

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Erythropoietin Induces an Epithelial to Mesenchymal Transition-Like Process in Mammary Epithelial Cells MCF10A

Ordoñez-Moreno

Rodriguez‐Monterrosas

Cortés‐Reynosa

et al. 2017

J. Cell. Biochem.

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Anemia is associated with chemotherapy treatment in cancer patients. Erythropoietin (EPO) has been used to treat anemia of cancer patients, because it stimulates erythropoiesis. However, treatment of breast cancer patients with EPO has been associated with poor prognosis and decrease of survival. Epithelial to mesenchymal transition (EMT) is a process by which epithelial cells are transdifferentiated to a mesenchymal state. It has been implicated in tumor progression, because epithelial cells acquire the capacity to execute the multiple steps of invasion/metastasis process. However, the role of EPO on EMT process in human mammary epithelial cells has not been studied. In the present study, we demonstrate that EPO promotes a decrease of E-cadherin expression, an increase of N-cadherin, vimentin, and Snail2 expression, activation of FAK and Src kinases and an increase of MMP-2 and MMP-9 secretions. Moreover, EPO induces an increase of NFκB DNA binding activity, an increase of binding of p50 and p65 NFκB subunits to Snail1 promoter, migration, and invasion in mammary non-tumorigenic epithelial cells MCF10A. In summary, these findings demonstrate, for the first time, that EPO induces an EMT-like process in mammary non-tumorigenic epithelial cells. J. Cell. Biochem. 118: 2983-2992, 2017. © 2017 Wiley Periodicals, Inc.

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“…Comparisons were made to unstimulated cells. Ã P < 0.05. cells [Park et al, 2014[Park et al, , 2015. Our findings support our proposal that EPO induces an EMT process in MCF10A cells.…”

Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 91%

See 1 more Smart Citation

Erythropoietin Induces an Epithelial to Mesenchymal Transition-Like Process in Mammary Epithelial Cells MCF10A

Ordoñez-Moreno

Rodriguez‐Monterrosas

Cortés‐Reynosa

et al. 2017

J. Cell. Biochem.

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“… 9 The inhibitory effects of U0126 on MEK and ERK activation have been confirmed repeatedly, and treatments with U0126 have been shown to inhibit proliferation and migration of cancer cells in vivo and in vitro. 10 − 12…”

mentioning

confidence: 99%

U0126 Protects Cells against Oxidative Stress Independent of Its Function as a MEK Inhibitor

Ong

Guo

Zhang

et al. 2015

ACS Chem. Neurosci.

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U0126 is a potent and selective inhibitor of MEK1 and MEK2 kinases. It has been widely used as an inhibitor for the Ras/Raf/MEK/ERK signaling pathway with over 5000 references on the NCBI PubMed database. In particular, U0126 has been used in a number of studies to show that inhibition of the Raf/MEK/ERK pathway protects neuronal cells against oxidative stress. Here, we report that U0126 can function as an antioxidant that protects PC12 cells against a number of different oxidative-stress inducers. This protective effect of U0126 is independent of its function as a MEK inhibitor, as several other MEK inhibitors failed to show similar protective effects. U0126 reduces reactive oxygen species (ROS) in cells. We further demonstrate that U0126 is a direct ROS scavenger in vitro, and the oxidation products of U0126 exhibit fluorescence. Our finding that U0126 is a strong antioxidant signals caution for its future usage as a MEK inhibitor and for interpreting some previous results.

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“…Recently Ma et al (10) illustrated that SUMO-specific protease 1 regulates the proliferation and invasion of pancreatic cancer cells through MMP-9. Park et al (11) Mangiferin, also named as mango element or chinonin, is a natural polyphenolic compound extracted from the liliaceous plant, Anemarrhena. Modern pharmacological and clinical studies have shown that mangiferin has physiological activity and pharmacological effects in many aspects (12).…”

Section: Introductionmentioning

confidence: 99%

Mangiferin regulates proliferation and apoptosis in glioma cells by induction of microRNA-15b and inhibition of MMP-9 expression

et al. 2015

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Abstract. Mangiferin, a flavonoid extracted from the leaves of the Anacardiaceae plant, the mango tree, has physiological activity and pharmacological effects in many aspects. The present study aimed to clarify the effect of mangiferin on proliferation and apoptosis of glioma cells and the mechanism of these curative effects of mangiferin. In this experiment, we detected the proliferation using 3-(4,5-dimethylthylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay. Then, cell apoptosis of U87 glioma cells was measured with the Annexin V-FITC/propidium iodide (PI) apoptosis detection kit, DAPI staining assay and the caspase-3 and caspase-9 activity assay kit. Next, quantitative real-time PCR and gelatin zymography were used to analyze the expression of microRNA-15b (miR-15b) and matrix metalloproteinase-9 (MMP-9), respectively. MMP-9 agonist, miR-15b mimics and anti-miR-15b mimics were added to the U87 glioma cells for elucidating the mechanisms involved in the curative effects of mangiferin. In the present study, mangiferin notably restrained the proliferation and increased the apoptosis of the U87 glioma cells. Meanwhile, mangiferin specifically promoted the expression of miR-15b and suppressed the level of MMP-9 in the U87 glioma cells. miR-15b regulated the expression of MMP-9 in the U87 glioma cells. MMP-9 agonist and antimiR-15b reduced the curative effects of mangiferin in the U87 glioma cells. In summary, mangiferin regulates proliferation and apoptosis in glioma cells by induction of miR-15b and inhibition of MMP-9 expression.

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EPO gene expression induces the proliferation, migration and invasion of bladder cancer cells through the p21WAF1-mediated ERK1/2/NF-κB/MMP-9 pathway

Cited by 10 publications

References 30 publications

Erythropoietin Induces an Epithelial to Mesenchymal Transition-Like Process in Mammary Epithelial Cells MCF10A

Erythropoietin Induces an Epithelial to Mesenchymal Transition-Like Process in Mammary Epithelial Cells MCF10A

U0126 Protects Cells against Oxidative Stress Independent of Its Function as a MEK Inhibitor

Mangiferin regulates proliferation and apoptosis in glioma cells by induction of microRNA-15b and inhibition of MMP-9 expression

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