Ye Lin, Sanders Andrew J, Sun Ping-Hui, Mason Malcolm D, Jiang Wen G
Metastasis and Angiogenesis Research Group, Institute of Cancer and Genetics, Cardiff University School of Medicine, Cardiff CF14 4XN, UK.
Oncol Lett. 2014 Jun;7(6):2149-2153. doi: 10.3892/ol.2014.2038. Epub 2014 Apr 4.
Capillary morphogenesis gene 2 (CMG2), also known as anthrax toxin receptor 2, has been indicated in the formation of new vasculature and in the internalisation of the anthrax toxin. Anti-angiogenesis therapy that targets this molecule has been investigated. However, our recent studies of this molecule have indicated that this gene may also play certain roles in cancer cells. The present study aimed to examine the expression of CMG2 in prostate cancer tissues and cell lines, and also its impact on cellular functions. The expression of CMG2 was detectable in normal and prostate cancer tissues. The prostate cancer cell lines appeared to have relatively high expression compared with the prostatic epithelial cells. Knockdown of CMG2 impaired the adherence of the prostate cancer cells. CMG2 overexpression resulted in decreasing invasiveness, while the knockdown of CMG2 contrastingly enhanced this ability. The altered expression of CMG2 in the prostate cancer cells did not affect the or growth of the cells. Taken together, these results show that CMG2 is expressed in prostatic epithelia and cancer cells. In addition to its role in the angiogenesis and the internalisation of anthrax toxin, CMG2 also plays an important role in regulating the adhesion and invasion of prostate cancer cells.
毛细血管形态发生基因2(CMG2),也被称为炭疽毒素受体2,已被证实参与新血管形成以及炭疽毒素的内化过程。针对该分子的抗血管生成疗法已得到研究。然而,我们最近对该分子的研究表明,这个基因可能在癌细胞中也发挥着某些作用。本研究旨在检测CMG2在前列腺癌组织和细胞系中的表达情况,以及其对细胞功能的影响。在正常组织和前列腺癌组织中均可检测到CMG2的表达。与前列腺上皮细胞相比,前列腺癌细胞系似乎具有相对较高的表达。敲低CMG2会损害前列腺癌细胞的黏附能力。CMG2过表达导致侵袭性降低,而敲低CMG2则相反地增强了这种能力。前列腺癌细胞中CMG2表达的改变并不影响细胞的增殖或生长。综上所述,这些结果表明CMG2在前列腺上皮细胞和癌细胞中均有表达。除了在血管生成和炭疽毒素内化过程中的作用外,CMG2在调节前列腺癌细胞的黏附与侵袭方面也起着重要作用。