Overexpression of 伪v尾6 Integrin Alters the Colorectal Cancer Cell Proteome in Favor of Elevated Proliferation and a Switching in Cellular Adhesion That Increases Invasion
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- 作者：David Cantor ; Iveta Slapetova ; Alison Kan ; Leon R. McQuade ; Mark S. Baker
- 刊名：Journal of Proteome Research
- 出版年：2013
- 出版时间：June 7, 2013
- 年：2013
- 卷：12
- 期：6
- 页码：2477-2490
- 全文大小：545K
- 年卷期：v.12,no.6(June 7, 2013)
- ISSN：1535-3907
文摘
Many proteins enhance cancer progression toward life-threatening metastases. These include linking proteins called integrins that mediate cell adhesion to the extracellular matrix (ECM), consequently altering both function and phenotype. Specific neoexpression of the 尾6 integrin subunit correlates with the epithelial-to-mesenchymal transition, metastasis, and poor overall patient survival. While 尾6 is implicated in these processes, exactly how it affects signaling and/or proteolytic pathways in metastasis remains unclear. A membrane-enriched peptide immobilized pH gradient isoelectric focusing (IPG-IEF) shotgun proteomics study was undertaken in which subclones of the SW480 colorectal cancer cell line transfected with a vector inducing unregulated 尾6 integrin overexpression were compared with the 鈥渆mpty鈥?mock vector control cell line. 尾6 overexpression induced a significant change in 708 proteins and was found to be localized across most intracellular locations, some involving cellular processes and pathways underpinning cancer progression. Proteomics data have been deposited to the ProteomeXchange with identifier PXD000230. 尾6 expression increased cell proliferation 4-fold while decreasing cell adhesion to many integrin ECM substrates. 尾6 expression also enhanced cell invasion and promoted the expression/repression of many established cancer-related pathways.