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Open AccessJournal ArticleDOI

EMT and inflammation: inseparable actors of cancer progression

TLDR
The interconnections between EMT programs and cellular and molecular actors of inflammation are described, and data linking the EMT/inflammation axis to metastasis is recapitulate.
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This article is published in Molecular Oncology.The article was published on 2017-07-01 and is currently open access. It has received 368 citations till now. The article focuses on the topics: Epithelial–mesenchymal transition & Cancer cell.

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Nrf2 Down-Regulation by Camptothecin Favors Inhibiting Invasion, Metastasis and Angiogenesis in Hepatocellular Carcinoma.

TL;DR: In this article, the authors used EPI and Camptothecin (CPT) to determine the invasion and metastasis in Huh7 cells, H22 and Huh7 mouse models, and found that Nrf2 expression and ROS level were increased after incubation with EPI by western blot and flow cytometry assay.
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IL-6 Contributes to the TGF-β1-Mediated Epithelial to Mesenchymal Transition in Human Salivary Gland Epithelial Cells

TL;DR: The data collected demonstrate that IL-6 can induce SGEC to undergo a morphological and phenotypical transition to a mesenchymal phenotype, in a dose-dependent manner, and corroborate the hypothesis that dysregulated cytokines IL- 6 may contribute to the EMT-dependent fibrosis.
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In vitro and bioinformatics mechanistic-based approach for cadmium carcinogenicity understanding

TL;DR: The systematic analysis of up- and down-regulated transcripts and the comparison of DEGs in transformed cells evidence different functional targets and the complex picture of cadmium-induced transformation, including the switching-off of specific functions plays a major role in this process.
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The Role of the Innate Immune System in Cancer Dormancy and Relapse.

TL;DR: In this paper, a review follows the journey of metastatic cells from dissemination to dormancy and the onset of the metastatic outgrowth and recurrent tumor development, with emphasis on the role of the innate immune system.
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Epithelial–mesenchymal transition: role in cancer progression and the perspectives of antitumor treatment

TL;DR: This review examines the most recent data on the intracellular and extracellular molecular mechanisms that activate EMT and the role they play in various aspects of tumor progression, such as metastasis, apoptotic resistance, and immune evasion.
References
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Journal ArticleDOI

Monocyte chemoattractant protein-1 (MCP-1): an overview.

TL;DR: This review will discuss the biological processes and the structure and function of CCL2, one of the key chemokines that regulate migration and infiltration of monocytes/macrophages.
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Evidence for a tumoral immune resistance mechanism based on tryptophan degradation by indoleamine 2,3-dioxygenase

TL;DR: It is shown that most human tumors constitutively express IDO, and that expression of IDO by immunogenic mouse tumor cells prevents their rejection by preimmunized mice, suggesting that the efficacy of therapeutic vaccination of cancer patients might be improved by concomitant administration of an IDO inhibitor.
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Circulating Breast Tumor Cells Exhibit Dynamic Changes in Epithelial and Mesenchymal Composition

TL;DR: A role for EMT in the blood-borne dissemination of human breast cancer is supported as both single cells and multicellular clusters, expressing known EMT regulators, including transforming growth factor (TGF)–β pathway components and the FOXC1 transcription factor.
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Epithelial-to-mesenchymal transition is dispensable for metastasis but induces chemoresistance in pancreatic cancer

TL;DR: This study functionally probes the role of EMT in PDAC by generating mouse models of PDAC with deletion of Snail or Twist, two key transcription factors responsible for EMT, and highlights the importance of combining EMT inhibition with chemotherapy for the treatment of pancreatic cancer.
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Epithelial-to-mesenchymal transition is not required for lung metastasis but contributes to chemoresistance

TL;DR: The potential of an EMT-targeting strategy, in conjunction with conventional chemotherapies, for breast cancer treatment is suggested, using a mesenchymal-specific Cre-mediated fluorescent marker switch system in spontaneous breast-to-lung metastasis models.
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