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Critical Reviews™ in Immunology

Publicou 6 edições por ano

ISSN Imprimir: 1040-8401

ISSN On-line: 2162-6472

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.3 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.6 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00079 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

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The Activated NF-κB-Snail-RKIP Circuitry in Cancer Regulates Both the Metastatic Cascade and Resistance to Apoptosis by Cytotoxic Drugs

Volume 29, Edição 3, 2009, pp. 241-254
DOI: 10.1615/CritRevImmunol.v29.i3.40
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RESUMO

Premalignant cells acquire a series of genetic and epigenetic changes that are responsible for cell proliferation in the absence of growth factors. It is not yet defined how the initial steps of the invasive metastatic cascade are acquired. New insights into the initial steps of the metastatic process were revealed by a set of regulators that induced the differentiation program termed "the epithelial to mesenchymal transition (EMT)." EMT is regulated by distinct transcription factors such as Snail, Slug and TWIST. Overexpression of Snail in cancer is responsible, in part, for the induction of EMT through the downregulation of E-cadherin and cytokeratins and the induction of mesenchymal protein expression such as vimentin, fibronectin, N-cadherin, metalloproteases, and invasiveness. In contrast, the metastatic suppressor Raf-kinase inhibitor protein (RKIP) is poorly expressed in primary cancers and absent in various metastatic cancers. RKIP inhibits NF-κB activity through direct interaction with NIK and TAK1. Snail was shown to suppress RKIP transcription and expression, and Snail is transcriptionally regulated by NF-κB. Thus, a circuitry is developed in which overexpression of Snail in tumors inhibits RKIP and induces EMT. In addition, NF-κB, Snail, and RKIP have been shown to regulate tumor-cell resistance to apoptotic stimuli. Inhibition of NF-κB and Snail and induction of RKIP sensitize resistant tumor cells to apoptosis by various chemotherapeutic and immunotherapeutic drugs. Furthermore, the ratio of Snail over RKIP expression in tumor cells is of prognostic significance and predicts response to cytotoxic therapies. Thus, pharmacological agents regulating the RKIP-NF-κB-Snail loop can be used as both sensitizing agents for apoptosis when combined with cytotoxic therapies as well as inhibitors of metastasis.

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