Tumor suppressive role of an androgen-regulated epithelial cell adhesion molecule (C-CAM) in prostate carcinoma cell revealed by sense and antisense approaches.
Tumor suppressive role of an androgen-regulated epithelial cell adhesion molecule (C-CAM) in prostate carcinoma cell revealed by sense and antisense approaches.
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发表时间：
1995
期刊：
影响因子：
11.2
通讯作者：
J. Hsieh;W. Luo;Weitao Song;Yang Wang;D. Kleinerman;Nguyen T. Van;S. Lin
中科院分区：
文献类型：
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作者：
J. Hsieh;W. Luo;Weitao Song;Yang Wang;D. Kleinerman;Nguyen T. Van;S. Lin
我们最近证明C-CAM是免疫球蛋白超基因家族的上皮细胞粘附分子，可受雄激素调节，并可能在前列腺上皮分化过程中起生长抑制作用。为了确定C-CAM在前列腺肿瘤发生中的作用，我们用含有C-CAM1 （C-CAM亚型）的表达质粒转染了致瘤性人前列腺癌细胞PC-3。与对照细胞相比，转染后的克隆表现出明显较低的生长速率、不依赖于锚定的生长和较低的体内致瘤性。此外，将反义载体转染到非致瘤性前列腺上皮细胞系NbE中，导致裸鼠肿瘤形成。来自这些nbe诱导肿瘤的亚线细胞的C-CAM水平低于对照细胞。这些数据表明C-CAM1在前列腺肿瘤发生中可以作为肿瘤抑制因子发挥作用。
We recently demonstrated that C-CAM, an epithelial-cell adhesion molecule of the immunoglobulin supergene family, could be regulated by androgen and might act as a growth repressor during differentiation of the prostatic epithelium. To define the role of C-CAM in prostatic tumorigenesis, a tumorigenic human prostatic cancer cell line, PC-3, was transfected with an expression plasmid containing C-CAM1 (a C-CAM isoform). Transfected clones showed significantly lower growth rates, reduced anchorage-independent growth, and less tumorigenicity in vivo than control cells. Furthermore, transfection of an antisense vector into a nontumorigenic prostatic epithelial cell line, NbE, resulted in tumor formation in nude mice. Sublines derived from these NbE-induced tumors had lower levels of C-CAM than did control cells. These data suggest that C-CAM1 can function as a tumor suppressor in prostate tumorigenesis.