CD90 is a glycophosphatidylinositol (GPI)-anchored glycoprotein, which is highly expressed in stem cells. CD90 involves in immunological function and nonimmunological functions, including cell adhesion, migration and cell death. The published data show that CD90 is a tumor suppressor gene in ovarian cancer and nasopharyngeal carcinoma. However, several studies indicate that CD90 is a potential marker for liver cancer stem cells (CSCs). It suggests that CD90 leads to different function in different tumors. In order to elucidate the role of CD90 in liver cancer progression, the HepG2 and Hep3B stable transfectants expressing exogenous CD90 were established and the tumorigenic ability was analyzed in vivo and in vitro. We further analyzed the stemness properties of the transfectants and found that CD90 increased the sphere formation ability and ALDH activity. We further analyzed the role of CD90 in ovarian cancer cell and found that there is a controversial phenotype in SKOV3 cell compared to liver cancer cell. Several cell surface markers have been used to identify liver cancer stem cells including CD90, EpCAM, CD133, CD44, and CD13. Among these markers, CD90 is particularly interesting since overexpression of CD90 inhibited the growth of another type of tumor. We analyzed the cross-talk interaction between CD90 and the other CSC markers and found that there was a cause-effect relationship. We further identified the signaling transduction pathway in mediating the processes of CD90-induced tumorigenic ability. Our findings provide a concept to target stemness-associated signaling axis as a strategy to treat cancer.
Citation Format: Wei-Ching Chen, Ming-Derg Lai. Study on cancer stem cell marker CD90 in liver cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1389. doi:10.1158/1538-7445.AM2015-1389