TGF<i>β</i>Signaling in Tumor Initiation, Epithelial-to-Mesenchymal Transition, and Metastasis

Papageorgis, Panagiotis

doi:10.1155/2015/587193

Cited by 194 publications

(170 citation statements)

References 220 publications

(193 reference statements)

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“…For example, transforming growth factor b (TGFb) plays multifunctional roles in the regulation of cell behavior, and is implicated in both developmental biology and cancer biology. 20,21 TGFb is noteworthy for its paradoxical actions, having both inhibitory and stimulatory effects on cell growth. 22 In the early stages of cancer, TGFb acts as a growth inhibitor and tumor-suppressor; but in the later stages, it can act as a potent inducer of EMT.…”

Section: Inducers Of Emtmentioning

confidence: 99%

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

Davies

Pollheimer

Yong

et al. 2016

Cell Adhesion & Migration

213

146

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A successful pregnancy depends on the intricate and timely interactions of maternal and fetal cells. Placental extravillous cytotrophoblast invasion involves a cellular transition from an epithelial to mesenchymal phenotype. Villous cytotrophoblasts undergo a partial epithelial to mesenchymal transition (EMT) when differentiating into extravillous cytotrophoblasts and gain the capacity to migrate and invade. This review summarizes our current knowledge regarding known regulators of EMT in the human placenta, including the inducers of EMT, upstream transcription factors that control EMT and the downstream effectors, cell adhesion molecules and their differential expression and functions in pregnancy pathologies, preeclampsia (PE) and fetal growth restriction (FGR). The review also describes the research strategies that were used for the identification of the functional role of EMT targets in vitro. A better understanding of molecular pathways driven by placental EMT and further elucidation of signaling pathways underlying the developmental programs may offer novel strategies of targeted therapy for improving feto-placental growth in placental pathologies including PE and FGR.

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Section: Inducers Of Emtmentioning

confidence: 99%

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

Davies

Pollheimer

Yong

et al. 2016

Cell Adhesion & Migration

213

146

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“…TGF-β exists in at least three isoforms: TGF-β1, TGF-β2, and TGF-β3. [110] In the TGF-β superfamily, only TGF-β1, produced by activated microglia, and TGF-β2, produced by astrocytes and neurons. [111] TGF-β1 and TGF-β2 increased prominently after ischemic stroke.…”

Section: Il-1βmentioning

confidence: 99%

Role of neuroinflammation in ischemic stroke

Li¹,

Pan²,

Tang³

et al. 2017

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Ischemic stroke causes the depletion of energy and induce excitotoxicity and neuroinflammation in the brain that results from thrombotic blockage. Neuroinflammation occurs initially depending on activated resident microglia that has the same function as the macrophage. Activated microglia participates in the neuroinflammatory process by phagocytosing the injured brain cells and producing the pro-and anti-inflammatory mediators. In this review, the authors present an overview of the role of microglia in mediating neuroinflammation in ischemic stroke. Key words:Microglia, ischemic stroke, neuroinflammation ABSTRACT Topic: StrokeThis is an open access article distributed under the terms of the Creative Commons AttributionNonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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“…The transforming growth factor β (TGF-β) plays crucial roles in cell proliferation, differentiation, invasion, apoptosis, epithelial-mesenchymal transition (EMT), and metastasis in cancer cells [8]. And these functions mainly happen through TGF-β binding to 2 types of cell-surface transmembrane serine/threonine kinase receptors (TGF-β receptor types 1 and 2), and subsequent activation of SMAD-dependent and -independent signaling pathways [9].…”

Section: Introductionmentioning

confidence: 99%

“…Treatment of exogenous TGF-β reduces sensitivity to cisplatin in A549 cells, and inhibition of the TGF-β pathway restores confluence-dependent resistance to cisplatin in A549 cells [10], while the molecular mechanism of TGF-β-induced inhibition of sensitivity to cisplatin is still elusive. Accumulated evidences indicated that TGF-β stimulates various genes expression in lung fibroblast and epithelium during fibrogenesis [11], lung injury [12,] and tumorigenesis [8]. Among those genes, heat-shock protein 27 (HSP27), has been identified as an important regulator involved in the development of various cancers and chemoresistance during drug treatment [13,14,15].…”

Section: Introductionmentioning

confidence: 99%

Heat Shock Protein 27, a Novel Regulator of Transforming Growth Factor β Induced Resistance to Cisplatin in A549 Cell

Huang

Yang²,

Sun³

et al. 2017

Pharmacology

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Lung cancer is one of the major causes of cancer morbidity and mortality around the world, and the resistance to cisplatin is a critical issue to chemotherapy in lung cancer patients. Transforming growth factor β (TGF-β) signal pathway abnormality is widely observed in drug resistance during lung cancer chemotherapy. Here, we investigated the effects of heat-shock protein 27 (HSP27) in the TGF-β-induced cisplatin resistance in lung cancer cell. In this study, our results indicated that the mRNA and protein expression of HSP27 were significantly increased in human lung cancer tissues. TGF-β induced the mRNA and protein expression of HSP27 in human lung cancer cell (A549). Treatment of TGF-β-induced cisplatin resistance in A549 cell through blocking the cisplatin-induced apoptosis and cell death, which characterized as the increasing of cell viability and decreasing of PARP and caspase3 cleavage in the cisplatin-treated cell. Knockdown of SMAD3 attenuated the TGF-β-induced HSP27 expression and restored the TGF-β-induced cisplatin resistance in A549 cell. Additionally, the knockdown of HSP27 blocked TGF-β-induced cisplatin resistance via decreasing cell viability and increasing cell apoptosis in A549 cell. These data therefore suggested that HSP27 is critical to lung cancer progression and TGF-β-induced cisplatin resistance in human lung cancer cell, and may provide an effective clinical strategy in lung cancer patients with resistance to chemotherapy.

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TGFβSignaling in Tumor Initiation, Epithelial-to-Mesenchymal Transition, and Metastasis

Cited by 194 publications

References 220 publications

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

Role of neuroinflammation in ischemic stroke

Heat Shock Protein 27, a Novel Regulator of Transforming Growth Factor β Induced Resistance to Cisplatin in A549 Cell

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