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Carbonic anhydrase‐related protein VIII promotes colon cancer cell growth
Author(s) -
Nishikata Makoto,
Nishimori Isao,
Taniuchi Keisuke,
Takeuchi Tamotsu,
Minakuchi Tomoko,
Kohsaki Takuhiro,
Adachi Yoshihiro,
Ohtsuki Yuji,
Onishi Saburo
Publication year - 2007
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.20264
Subject(s) - biology , colorectal cancer , cell growth , cell culture , gene knockdown , cancer research , microbiology and biotechnology , in vitro , transfection , in vivo , cell , carbonic anhydrase ii , carbonic anhydrase , cancer , enzyme , biochemistry , genetics
Increased expression of carbonic anhydrase‐related protein (CA‐RP) VIII has previously been shown in colorectal carcinoma. Since CA‐RP has no catalytic carbonic anhydrase (CA) activity, the present study attempted to elucidate its biological significance in colon cancer cells. From a colon cancer cell line (LoVo), we established clones that overexpressed CA‐RP VIII (LoVo‐CA8) and a control transfectant with a vector alone (LoVo‐pCIneo) and studied alterations in the biological behaviors of the tumor cells both in vitro and in vivo. LoVo‐CA8 cells showed significantly increased mRNA and protein expressions of CA‐RP VIII as compared to LoVo‐pCIneo cells. Cell proliferation, colony formation, and cell invasion assays showed that LoVo‐CA8 cells had significantly higher cell proliferative and invasive abilities as compared to parental LoVo and LoVo‐pCIneo cells in vitro. In an in vivo xenograft assay, LoVo‐CA8 cells showed a higher tumor growth rate than parental LoVo cells. Further, small interfering RNA (siRNA)‐mediated knockdown of CA‐RP VIII revealed significant inhibition in cell proliferation and colony formation of a colon cancer cell line HCT116, which showed high endogenous expression of CA‐RP VIII. These findings indicated that CA‐RP VIII plays a role in the growth of colon cancer cells. © 2007 Wiley‐Liss, Inc.