Inhibition of cell migration by ouabain in the A549 human lung cancer cell line

Liu, Ning; Li, Yali; Su, Suwen; Wang, Na; Wang, Huici; Li, Junxia

doi:10.3892/ol.2013.1406

Cited by 42 publications

(40 citation statements)

References 25 publications

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“…The antimetastasis is one of the chemotheraptic function for anti‐cancer drugs . Numerous evidence have shown that ouabain also induced cytotoxic effects including induction of cancer cell apoptosis and inhibited cancer cell migration and invasion of human liver cancer A549 cells; however, there is no report to show ouabain inhibiting migration and invasion and altered associated gene expression in human bone cancer cells. Herein, we investigated the effects of ouabain on migration and invasion of human osteosarcoma U‐2 OS cells in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…Ouabain at physiological concentrations is able to inhibit the migratory activities of human lung cancer H292 cells . Ouabain inhibited the epidermal growth factor (EGF)‐enhanced migration of A549 cells and the basal migration of A549 cells in the absence of EGF . Ouabain inhibited cell migration in A549 cells appear to be related to its ability to regulate and inactivate Src‐to‐ezrin signaling …”

Section: Introductionmentioning

confidence: 99%

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Ouabain impairs cell migration, and invasion and alters gene expression of human osteosarcoma U‐2 OS cells

Shih¹,

Liu³

et al. 2017

Environmental Toxicology

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Ouabain, the specific Na /K -ATPase blocker, has biological activity including anti-proliferative and anti-metastasis effects in cancer cell. There is no study to show ouabain inhibiting cell migration and invasion in human osteosarcoma U-2 OS cells. Thus, we investigated the effect of ouabain on the cell migration and invasion of human osteosarcoma U-2 OS cells. Results indicated that ouabain significantly decreased the percentage of viable cells at 2.5-5.0 μM, thus, we selected 0.25-1.0 μM for inhibiting studies. Ouabain inhibited cell migration, invasion and the enzymatic activities of MMP-2, and also affected the expression of metastasis-associated protein in U-2 OS cells. The cDNA microarray assay indicated that CDH1, TGFBR3, SHC3 and MAP2K6 metastasis-related genes were increased, but CCND1, JUN, CDKN1A, TGFB1, 2 and 3, SMAD4, MMP13, MMP2 and FN1 genes were decreased. These findings provide more information regarding ouabain inhibited cell migration and invasion and associated gene expressions in U-2 OS cells after exposed to ouabain.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ouabain impairs cell migration, and invasion and alters gene expression of human osteosarcoma U‐2 OS cells

Shih¹,

Liu³

et al. 2017

Environmental Toxicology

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“…Thus, EGFR signaling mediates the initial stages of EMT and EGFR inhibition may restrain EMT in certain cellular contexts. In support of this hypothesis, ligand-independent, constitutively active forms of EGFR can increase motility and invasiveness of tumor cells and EGFR inhibitors block cancer cell migration in vitro (Liu et al , 2013; Yue et al , 2012)…”

Section: Hallmarks Of Transformationmentioning

confidence: 89%

Epidermal Growth Factor Signaling in Transformed Cells

Lindsey

Langhans

2015

International Review of Cell and Molecular Biology

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Members of the epidermal growth factor receptor (EGFR/ErbB) family play a critical role in normal cell growth and development. However, many ErbB family members, especially EGFR, are aberrantly expressed or deregulated in tumors and are thought to play crucial roles in cancer development and metastatic progression. In this chapter, we provide an overview of key mechanisms contributing to aberrant EGFR/ErbB signaling in transformed cells which results in many phenotypic changes associated with the earliest stages of tumor formation, including several hallmarks of epithelial-to-mesenchymal transition (EMT). These changes often occur through interaction with other major signaling pathways important to tumor progression resulting in a multitude of transcriptional changes that ultimately impact cell morphology, proliferation and adhesion, all of which are crucial for tumor progression. The resulting mesh of signaling networks will need to be taken into account as new regimens are designed for targeting EGFR for therapeutic intervention. As new insights into the molecular mechanisms of the cross-talk of EGFR signaling with other signaling pathways and their role in therapeutic resistance to anti-EGFR therapies are gained a continual reassessment of clinical therapeutic regimes and strategies will be required. Understanding the consequences and complexity of EGF signaling and how it relates to tumor progression is critical for the development of clinical compounds and establishing clinical protocols for the treatment of cancer.

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“…A previous study reported that ouabain, a cardioactive glycoside, impedes invasion by decreasing the basal and enhanced migration in human lung cancer A549 cells 28 . Interestingly, it is observed that CK strongly inhibits the motility of lung cancer cells with or without EGF-stimulation ( Figure 5), suggesting that this might be an antimigratory activity of CK.…”

mentioning

confidence: 99%

“…Three hours later, each well was scratched using 10 l plastic pipette tip and washed with PBS. The medium was replaced with control medium or EGF-medium, following our treatment schedules (2% FBS, 2% FBS + EGF, 2% FBS + 50 M of CK, 2% FBS+ E GF + 50 M of CK) 28 . To quantify the scratched region, four randomly selected areas were photographed at  10 under an optical microscope (Eclipse ME600L, Nikon Instruments, NJ, USA).…”

mentioning

confidence: 99%

The Inhibitory Mechanism of Compound K on A549 Lung Cancer Cells through EGF Pathway:An <i>in Silico</i> and <i>in Vitro</i> Approach

Castro-Aceituno¹,

Ṣiddiqi²,

Ahn³

et al. 2016

Current Science

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In previous studies compound K (CK), an active metabolite ginsenoside from Panax ginseng, was shown to exhibit anti-cancer activity. However, the mechanism of CK through the EGFR/H-Ras pathway in cancer cells has not been reported so far. Therefore, we focused on the effect of CK as an EGFR and H-Ras inhibitor by in silico and in vitro studies using A549 cells. The biological activity prediction shows that CK exhibits chemopreventive, anticarcinogenic and antimetastatic activity. Also, using molecular docking studies it has been shown that CK exhibits a strong binding energy with EGFR and H-Ras than Erlotinib. CK inhibits cell viability, decreases cell migration, induces apoptosis and strongly decreases gene expression of EGFR and H-Ras genes in vitro. This finding suggests that the EGFR pathway is involved in the anti-cancer activity of CK of EGF-enhanced A549 lung cancer cell line.

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Inhibition of cell migration by ouabain in the A549 human lung cancer cell line

Cited by 42 publications

References 25 publications

Ouabain impairs cell migration, and invasion and alters gene expression of human osteosarcoma U‐2 OS cells

Ouabain impairs cell migration, and invasion and alters gene expression of human osteosarcoma U‐2 OS cells

Epidermal Growth Factor Signaling in Transformed Cells

The Inhibitory Mechanism of Compound K on A549 Lung Cancer Cells through EGF Pathway:An <i>in Silico</i> and <i>in Vitro</i> Approach

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