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Carbonic anhydrase IX (CA9) modulates tumor-associated cell migration and invasion

Authors
 Hye-Jin Shin ; Seung Bae Rho ; Joo-Young Kim ; Eok-Soo Oh ; Inn-Oc Han ; Dae Chul Jung 
Citation
 Journal of Cell Science, Vol.124(pt7) : 1077~1087, 2011 
Journal Title
 Journal of Cell Science 
ISSN
 0021-9533 
Issue Date
2011
Abstract
Expression of carbonic anhydrase IX (CA9) was shown to be strongly involved in high incidences of metastasis and poor prognosis in various human tumors. In this study, we investigated the possible role for CA9 in tumor metastases in vitro, using a gene transfection tool in the human cervical carcinoma cell line C33A. Gene expression profiling of CA9-transfected cells (C33A/CA9) and vector-transfected cells (C33A/Mock) was investigated by DNA microarray. The biological functions of differentially expressed genes between the C33A/CA9 and C33A/Mock cells included cell growth, regulation of cell-cell and cell-extracellular matrix adhesion and cytoskeletal organization. Immunofluorescent stain and Matrigel culture showed cytoskeletal remodeling, disassembled focal adhesion, weakened cell-cell adhesion and increased motility in C33A/CA9 cells. These invasive and metastatic phenotypes were associated with Rho-GTPase-related epithelial-mesenchymal transition. Inhibition of the Rho/Rho kinase pathway by a ROCK inhibitor (Y27632) and si-Rho (short interference RNA against RhoA) showed that Rho-GTPase signaling was involved in cellular morphologic and migratory changes. The effect of CA9 on Rho-GTPase signaling was also confirmed by silencing CA9 expression. Our results suggest that CA9 overexpression induces weakening of cell adhesions and augmented cell motility by aberrant Rho-GTPase signal transduction. Our study shows an underlying mechanism of CA9-related enhanced metastatic potential of tumor cells.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/94523
DOI
10.1242/jcs.072207
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Radiology
Yonsei Authors
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