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

期刊

PHYSIOLOGICAL GENOMICS
卷 46, 期 19, 页码 699-724

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiolgenomics.00062.2014

关键词

bioinformatics; cancer; epithelial-to-mesenchymal transition; EMT; NEDD9/HEF1; E-cadherin; SRC; TGF-beta; beta-catenin; genomics; proteomics; sequencing; precision oncology

资金

  1. National Cancer Institute [U54 CA-149147, R21 CA-181287, R01 CA-63366, P50 CA-083638, F30 CA-180607, CA-06927]

向作者/读者索取更多资源

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-beta (TGFB1), NEDD9/HEF1, beta-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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