FGF16 Promotes Invasive Behavior of SKOV-3 Ovarian Cancer Cells through Activation of Mitogen-activated Protein Kinase (MAPK) Signaling Pathway

Basu, Madhumita; Mukhopadhyay, Satinath; Chatterjee, Uttara; Roy, Sib Sankar

doi:10.1074/jbc.m113.535427

Cited by 42 publications

(53 citation statements)

References 48 publications

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“…Transient transfections with 1µg plasmid DNA were performed with Lipofectamine 2000 (Invitrogen) at 1: 3 ratio for 24-48 h. SIRT1 siRNA (Santa Cruz Biotechnology, USA) were used at 20 nM/2.5 × 10 5 cells with Lipofectamine 2000 (Invitrogen) for 48 h [21]. …”

Section: Methodsmentioning

confidence: 99%

Lysophosphatidic Acid Promotes Epithelial to Mesenchymal Transition in Ovarian Cancer Cells by Repressing SIRT1

Ray

Roy

Chowdhury

2017

Cell Physiol Biochem

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Background/Aims: Epithelial-to-mesenchymal transition (EMT) plays an essential role in the transition from early to invasive phenotype, however the underlying mechanisms still remain elusive. Herein, we propose a mechanism through which the class-III deacetylase SIRT1 regulates EMT in ovarian cancer (OC) cells. Methods: Expression analysis was performed using Q-PCR, western blot, immunofluorescence and fluorescence-IHC study. Matrigel invasion assay was used for the invasion study. Morphological alterations were observed by phalloidin-staining. Co-immunoprecipitation study was performed to analyze protein-protein interaction. Results: Overexpression of SIRT1-WT as well as Resveratrol-mediated SIRT1 activation antagonized the invasion of OC cells by suppressing EMT. SIRT1 deacetylates HIF1α, to inactivate its transcriptional activity. To further validate HIF1α inactivation, its target gene, i.e. ZEB1, an EMT-inducing factor was found to attenuate upon SIRT1 activation. To uncover the regulatory factor governing SIRT1 expression, lysophosphatidic acid (LPA), a highly enriched oncolipid in ascites/serum of OC patients, was found to down-regulate SIRT1 expression. Importantly, LPA was found to induce the mesenchymal switch in OC cells through suppression of SIRT1. Decreased level of SIRT1 was further validated in ovarian tissue samples of OC patients. Conclusion: We have identified a mechanism that relates SIRT1 down-regulation to LPA-induced EMT in OC cells and may open new arenas on developing novel anti-cancer therapeutics.

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Section: Methodsmentioning

confidence: 99%

Lysophosphatidic Acid Promotes Epithelial to Mesenchymal Transition in Ovarian Cancer Cells by Repressing SIRT1

Ray

Roy

Chowdhury

2017

Cell Physiol Biochem

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“…Several other signalling pathways are also known to induce EMT [9, 20, 21], Wnt signalling being one of them. Wnt functions by binding to the cell surface receptor Frizzled, which, in turn, inactivates Glycogen Synthase Kinase 3β (GSK3β), leading to stabilization of β-catenin [22], which translocates to the nucleus and upregulates the transcription of its target genes, many of which induce EMT.…”

Section: Introductionmentioning

confidence: 99%

Co-Activation of TGFβ and Wnt Signalling Pathways Abrogates EMT in Ovarian Cancer Cells

Mitra¹,

Roy²

2017

Cell Physiol Biochem

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Background/Aims: The aggressive property of ovarian cancer (OC) in terms of epithelial-mesenchymal transition (EMT), proliferation and metastasis are of major concern. Different growth factors including TGFβ are associated with regulating these molecular events but the underlying mechanisms remain unclear. The aim of this report is to decipher the regulation of EMT by co-activation of TGFβ and Wnt signalling cascades in gaining malignancy. Methods: The expression of the different components of signalling events were analyzed by QPCR, Western blot, Immunofluorescence microscopy and flow cytometry. β-catenin promoter activity was checked by luciferase assay. Results: We observed reduced EMT in ovarian cancer cells upon co-activation with TGFβ1 and LiCl as shown by the expressions of epithelial/mesenchymal markers and the EMT promoting factor, Snail1, accompanied by decrease in the invasion and migration of the cells compared to individual pathway activation. A detailed study of the mechanism suggested reduction in the β-catenin and p-GSK3b (Ser 9) levels to be the driving cause of this phenomenon, which was reversed upon co-activation with higher concentrations of LiCl. Conclusions: Therefore, tumourigenesis might be affected by the concentration of ligand/ growth factors for the respective signalling pathways activated in the tumour microenvironment and interaction between them might alter tumourigenesis.

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“…Therefore, there is increased interest in the discovery of novel diagnostic biomarkers [42,113] and in the identification of factors involved in cancer invasiveness and growth [114,115]. The implementation of metabolomics to study human biofluids and ovarian cyst fluids uncovers a decreased level of valine, alanine and phospholipids, and an increased level of ketone bodies in the serum of patients with ovarian carcinoma [116], together with an increase in isoleucine, valine, lysine, lactate and choline concentrations in malignant cyst fluids [117].…”

Section: Metabolomics and Ovarian Cancer Cell Linesmentioning

confidence: 99%

Metabolomics in cell culture—A strategy to study crucial metabolic pathways in cancer development and the response to treatment

Halama¹

2014

Archives of Biochemistry and Biophysics

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FGF16 Promotes Invasive Behavior of SKOV-3 Ovarian Cancer Cells through Activation of Mitogen-activated Protein Kinase (MAPK) Signaling Pathway

Cited by 42 publications

References 48 publications

Lysophosphatidic Acid Promotes Epithelial to Mesenchymal Transition in Ovarian Cancer Cells by Repressing SIRT1

Lysophosphatidic Acid Promotes Epithelial to Mesenchymal Transition in Ovarian Cancer Cells by Repressing SIRT1

Co-Activation of TGFβ and Wnt Signalling Pathways Abrogates EMT in Ovarian Cancer Cells

Metabolomics in cell culture—A strategy to study crucial metabolic pathways in cancer development and the response to treatment

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