Huang R P, Fan Y, Hossain M Z, Peng A, Zeng Z L, Boynton A L
Northwest Hospital, Seattle, Washington 98125, USA.
Cancer Res. 1998 Nov 15;58(22):5089-96.
Connexins (cx), structural components of gap junction, are believed to play a role in the regulation of cell proliferation and suppression of the neoplastic phenotype. We used human brain glioblastoma tumor cells as a model system to test this hypothesis. Western blot and reverse transcription-PCR analysis indicate that the expression levels of the gap junction protein connexin 43 (cx43) are profoundly decreased in several human brain tumor cell lines examined. Transfection of human cx43 into human glioblastoma cell lines U251 and T98G profoundly reduces cell proliferation in monolayer culture, in soft agar, and in athymic nude mice. Surprisingly, these effects are not associated with the establishment of gap junction communication in cx43 transfected cells. We conclude that the loss of cx43 expression may play a role in the development of human gliomas and that cx43 acts as a tumor suppressor gene to human glioblastoma.
连接蛋白（Cx）是间隙连接的结构成分，被认为在细胞增殖调控和肿瘤表型抑制中发挥作用。我们使用人脑胶质母细胞瘤肿瘤细胞作为模型系统来验证这一假设。蛋白质免疫印迹和逆转录-聚合酶链反应分析表明，在所检测的几种人脑肿瘤细胞系中，间隙连接蛋白连接蛋白43（Cx43）的表达水平显著降低。将人Cx43转染到人胶质母细胞瘤细胞系U251和T98G中，可显著降低单层培养、软琼脂培养以及无胸腺裸鼠体内的细胞增殖。令人惊讶的是，这些效应与Cx43转染细胞中间隙连接通讯的建立无关。我们得出结论，Cx43表达缺失可能在人类胶质瘤的发生发展中起作用，并且Cx43对人胶质母细胞瘤起肿瘤抑制基因的作用。
