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Bioinformatic approaches to augment study of epithelial-to-mesenchymal transition in lung cancer
Journal article   Open access   Peer reviewed

Bioinformatic approaches to augment study of epithelial-to-mesenchymal transition in lung cancer

Tim N Beck, Adaeze J Chikwem, Nehal R Solanki and Erica A Golemis
Physiological genomics, v 46(19), pp 699-724
01 Oct 2014
PMID: 25096367
url
https://doi.org/10.1152/physiolgenomics.00062.2014View
Published, Version of Record (VoR)Open Access (License Unspecified) Open

Abstract

Adaptor Proteins, Signal Transducing - genetics beta Catenin - genetics Cadherins - genetics Computational Biology - methods Computational Biology - trends Epithelial-Mesenchymal Transition - physiology Gene Expression Regulation, Neoplastic - genetics Gene Expression Regulation, Neoplastic - physiology Humans Lung Neoplasms - physiopathology Models, Biological Phosphoproteins - genetics Signal Transduction - genetics Signal Transduction - physiology Transforming Growth Factor beta1 - genetics
Bioinformatic approaches are intended to provide systems level insight into the complex biological processes that underlie serious diseases such as cancer. In this review we describe current bioinformatic resources, and illustrate how they have been used to study a clinically important example: epithelial-to-mesenchymal transition (EMT) in lung cancer. Lung cancer is the leading cause of cancer-related deaths and is often diagnosed at advanced stages, leading to limited therapeutic success. While EMT is essential during development and wound healing, pathological reactivation of this program by cancer cells contributes to metastasis and drug resistance, both major causes of death from lung cancer. Challenges of studying EMT include its transient nature, its molecular and phenotypic heterogeneity, and the complicated networks of rewired signaling cascades. Given the biology of lung cancer and the role of EMT, it is critical to better align the two in order to advance the impact of precision oncology. This task relies heavily on the application of bioinformatic resources. Besides summarizing recent work in this area, we use four EMT-associated genes, TGF-β (TGFB1), NEDD9/HEF1, β-catenin (CTNNB1) and E-cadherin (CDH1), as exemplars to demonstrate the current capacities and limitations of probing bioinformatic resources to inform hypothesis-driven studies with therapeutic goals.

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Collaboration types
Domestic collaboration
Web of Science research areas
Cell Biology
Genetics & Heredity
Physiology
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