EMT in carcinoma progression and dissemination: Facts, unanswered questions, and clinical considerations

Bastid, Jérémy

doi:10.1007/s10555-011-9344-6

Cited by 83 publications

(68 citation statements)

References 50 publications

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“…Additionally, we observed a significant decrease and increase in the expression of ERCC1 and p53, respectively, with the TNM stage of EC, which suggested ERCC1 and p53 as potential markers for the TNM stage of EC. EGFR overexpression was suggested to be associated with a number of cancers (Bastid, 2012); however, in this study, the expression of EGFR did not increase significantly with the TNM stage of EC, which suggested that the mechanisms of EC were unique, and that EGFR might be a key factor affecting this variation (Table 1). …”

Section: Association Between Ercc1 Egfr and P53 Expression And Clincontrasting

confidence: 62%

Effect of SNX-2112 on proliferation of esophageal cancer cells via regulation of excision repair cross-complementing 1, epidermal growth factor receptor, and p53 expression

Cy¹,

Ren²,

Yd³

2016

Genet. Mol. Res.

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ABSTRACT. SNX-2112 is a potential molecular targeted therapeutic drug against esophageal cancer (EC). However, its exact mechanism of action remains to be explained. The aim of this study was to investigate the effect of SNX-2112 on excision repair cross-complementing 1 (ERCC1), epidermal growth factor receptor (EGFR), and p53, to elucidate the mechanism of action of SNX-2112 on EC. Fresh tumor sections were surgically obtained from 65 patients with EC, and the expression of ERCC1, EGFR, and p53 was determined by immunohistochemical staining. Furthermore, the effect of SNX-2112 (0.2 µM) on the proliferation of EC-9706 cells and the expression of ERCC1, EGFR, and p53 in these cells were analyzed by a cell proliferation assay and western blot, respectively. We observed a significant decrease and increase in ERCC1 (P = 0.001) and p53 (P = 0.043) expression, respectively, and no significant difference in EGFR (P = 0.59) expression, with the TNM stage of EC, which suggested that ERCC1 and p53 could be potential markers for the TNM stage of EC. We also observed a significant increase in ERCC1 expression, and decrease in p53 and EGFR expression, in EC-9706 cells treated with SNX-2112 (P < 0.05), indicating the regulation of EC by SNX-2112. Furthermore, SNX-2112 treatment induced a significant decrease in the proliferation of EC-9706, which confirmed the function of SNX-2112. In summary, SNX-2112 inhibits the proliferation of EC cells by regulating the expression of ERCC1, EGFR, and p53.

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Section: Association Between Ercc1 Egfr and P53 Expression And Clincontrasting

confidence: 62%

Effect of SNX-2112 on proliferation of esophageal cancer cells via regulation of excision repair cross-complementing 1, epidermal growth factor receptor, and p53 expression

Cy¹,

Ren²,

Yd³

2016

Genet. Mol. Res.

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“…32,41 The agents tested in those studies were usually only for laboratory use. Recently, three COX-2 inhibitors have been reported to inhibit EMT in human bladder cancer cell lines in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Celecoxib attenuates hepatic cirrhosis through inhibition of epithelial‐to‐mesenchymal transition of hepatocytes

Wen

Gao

Yang

et al. 2014

J of Gastro and Hepatol

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Celecoxib could ameliorate hepatic fibrosis and cirrhosis in TAA-rat model through suppression of the mesenchymal biomarkers in the hepatocytes while restoring the levels of their epithelial biomarkers. The inhibitory effect of celecoxib on the EMT of hepatocytes is associated with reduction of intrahepatic inflammation, preservation of normal basement matrix, and inhibition of TGF-β1/Smad pathway.

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“…Moreover, once malignant carcinoma cells have metastasized to secondary sites, they can apparently revert back to epithelial-like morphologies along with reexpression of epithelial markers, indicating that EMT has transient and potentially reversible characteristics (80,81). Although EMT changes have been associated with invasion and metastasis in animal tumors, there remains an ongoing debate on whether this phenomenon is truly representative of malignant pathways in human cancers (84). Indeed, Tarin (85) has argued that invasive cell phenotypes occur after normal tissues are damaged and during embryogenesis and that there is a lack of convincing pathologic evidence in humans that EMT occurs when carcinomas metastasize.…”

Section: Cell Membranes and The Invasive Phenotypementioning

confidence: 99%

Cell Membrane Fluid–Mosaic Structure and Cancer Metastasis

Nicolson

2015

Cancer Research

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Cancer cells are surrounded by a fluid-mosaic membrane that provides a highly dynamic structural barrier with the microenvironment, communication filter and transport, receptor and enzyme platform. This structure forms because of the physical properties of its constituents, which can move laterally and selectively within the membrane plane and associate with similar or different constituents, forming specific, functional domains. Over the years, data have accumulated on the amounts, structures, and mobilities of membrane constituents after transformation and during progression and metastasis. More recent information has shown the importance of specialized membrane domains, such as lipid rafts, protein-lipid complexes, receptor complexes, invadopodia, and other cellular structures in the malignant process. In describing the macrostructure and dynamics of plasma membranes, membraneassociated cytoskeletal structures and extracellular matrix are also important, constraining the motion of membrane components and acting as traction points for cell motility. These associations may be altered in malignant cells, and probably also in surrounding normal cells, promoting invasion and metastatic colonization. In addition, components can be released from cells as secretory molecules, enzymes, receptors, large macromolecular complexes, membrane vesicles, and exosomes that can modify the microenvironment, provide specific cross-talk, and facilitate invasion, survival, and growth of malignant cells. Cancer Res; 75(7); 1169-76. Ó2015 AACR.

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EMT in carcinoma progression and dissemination: Facts, unanswered questions, and clinical considerations

Cited by 83 publications

References 50 publications

Effect of SNX-2112 on proliferation of esophageal cancer cells via regulation of excision repair cross-complementing 1, epidermal growth factor receptor, and p53 expression

Effect of SNX-2112 on proliferation of esophageal cancer cells via regulation of excision repair cross-complementing 1, epidermal growth factor receptor, and p53 expression

Celecoxib attenuates hepatic cirrhosis through inhibition of epithelial‐to‐mesenchymal transition of hepatocytes

Cell Membrane Fluid–Mosaic Structure and Cancer Metastasis

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