TY - JOUR
T1 - Homeobox gene HOPX is epigenetically silenced in human uterine endometrial cancer and suppresses estrogen-stimulated proliferation of cancer cells by inhibiting serum response factor
AU - Yamaguchi, Shinichiro
AU - Asanoma, Kazuo
AU - Takao, Tomoka
AU - Kato, Kiyoko
AU - Wake, Norio
N1 - Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.
PY - 2009/6/1
Y1 - 2009/6/1
N2 - HOPX (homeodomain only protein X) is a newly identified homeobox gene whose loss of expression has been reported for several types of neoplasm. Although we found most human uterine endometrial cancers (HEC) defective in HOPX expression, genetic mutations in the HOPX gene were undetectable. As is the case with several tumor suppressor genes, the promoter region of HOPX is densely methylated in HEC tissue samples obtained by laser capture microdissection. HOPX mRNA and protein levels were reduced in the majority of samples, and this correlated with hypermethylation of the HOPX promoter. Forced expression of HOPX resulted in a partial block in cell proliferation, in vivo tumorigenicity and c-fos gene expression in HEC and MCF7 cells in response to 17β-estradiol (E2) stimulation. Analysis of the serum response element (SRE) of c-fos gene promoter showed that the effect of HOPX expression is associated with inhibition of E2-induced c-fos activation through the serum response factor (SRF) motif. Knockdown of HOPX in immortalized human endometrial cells resulted in accelerated proliferation. Our study indicates that transcriptional silencing of HOPX results from hypermethylation of the HOP promoter, which leads to HEC development.
AB - HOPX (homeodomain only protein X) is a newly identified homeobox gene whose loss of expression has been reported for several types of neoplasm. Although we found most human uterine endometrial cancers (HEC) defective in HOPX expression, genetic mutations in the HOPX gene were undetectable. As is the case with several tumor suppressor genes, the promoter region of HOPX is densely methylated in HEC tissue samples obtained by laser capture microdissection. HOPX mRNA and protein levels were reduced in the majority of samples, and this correlated with hypermethylation of the HOPX promoter. Forced expression of HOPX resulted in a partial block in cell proliferation, in vivo tumorigenicity and c-fos gene expression in HEC and MCF7 cells in response to 17β-estradiol (E2) stimulation. Analysis of the serum response element (SRE) of c-fos gene promoter showed that the effect of HOPX expression is associated with inhibition of E2-induced c-fos activation through the serum response factor (SRF) motif. Knockdown of HOPX in immortalized human endometrial cells resulted in accelerated proliferation. Our study indicates that transcriptional silencing of HOPX results from hypermethylation of the HOP promoter, which leads to HEC development.
KW - 17β-estradiol
KW - DNA methylation
KW - HOPX
KW - Human uterine endometrial cancer
KW - Serum response factor
KW - Tumor suppressor gene
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U2 - 10.1002/ijc.24217
DO - 10.1002/ijc.24217
M3 - Article
C2 - 19173292
AN - SCOPUS:64249126794
SN - 0020-7136
VL - 124
SP - 2577
EP - 2588
JO - International Journal of Cancer
JF - International Journal of Cancer
IS - 11
ER -