Hsieh J T, Luo W, Song W, Wang Y, Kleinerman D I, Van N T, Lin S H
Department of Urology, University of Texas M. D. Anderson Cancer Center, Houston 77030.
Cancer Res. 1995 Jan 1;55(1):190-7.
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.
我们最近证实，免疫球蛋白超基因家族的上皮细胞粘附分子C-CAM可受雄激素调控，并可能在前列腺上皮细胞分化过程中作为生长抑制因子发挥作用。为了明确C-CAM在前列腺肿瘤发生中的作用，我们用含有C-CAM1（一种C-CAM同工型）的表达质粒转染了致瘤性人前列腺癌细胞系PC-3。与对照细胞相比，转染后的克隆显示出显著更低的生长速率、降低的非锚定依赖性生长能力以及在体内更低的致瘤性。此外，将反义载体转染至非致瘤性前列腺上皮细胞系NbE中，导致裸鼠体内形成肿瘤。源自这些NbE诱导肿瘤的亚系细胞中C-CAM水平低于对照细胞。这些数据表明，C-CAM1在前列腺肿瘤发生过程中可作为肿瘤抑制因子发挥作用。
