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  • Title: Promoting effects on the proliferation and metastasis of ACC tumor cell with XAGE-1b overexpression.
    Author: Zhou B, Li T, Liu Y, Zhu N.
    Journal: Oncol Rep; 2013 Nov; 30(5):2323-35. PubMed ID: 24008415.
    Abstract:
    Adenoid cystic carcinoma is salivary gland malignancy characterized by indolent yet relentless growth that exhibits inherent resistance to surgery, chemotherapy and radiotherapy and it also expresses genes associated with well-defined carcinogenic and metastasis processes. There is no clear role established for XAGE-1b, which is a member of the cancer testis antigen family in tumorigenesis and the metastasis process of ACC. We studied and elucidated the correlation between the proliferation and metastasis of ACC and XAGE-1b. The eukaryotic vector was constructed for XAGE-1b overexpression in ACC-2 cells, which were used for studying the proliferation and migration phenotype in vivo and in vitro. RNAi technology was used to suppress the expression of XAGE-1b in the ACC-M cell line, and shRNA expression vector was also constructed and screened for interfering XAGE-1b expression applied to ACC-M cell lines. The effects on cell migration activity with XAGE-1b overexpression were determined by QCMTM 24-Well Cell Invasion Assay in vitro, and a lung metastatic model in mice. We found decreased effects on the proliferation phenotype of ACC-M cell in vivo and in vitro with XAGE-1b downregulation, and XAGE-1b overexpression promoted the proliferation of ACC-2 cells in vivo and in vitro, while its overexpression promoted the transmembrane invasion of ACC-2 cells in vitro and metastasis in vivo of the nude mice. The proliferation in vitro of ACC-M cells and subcutaneous tumor growth of nude mice was inhibited by XAGE-1b interference. The ACC-2 cell line with XAGE-1b overexpression displayed more rapid proliferation and higher transmembrane and metastatic ability in vivo and in vitro, with more angiogenesis in the tumor tissues. XAGE-1b gene was able to influence angiogenesis directly or indirectly, leading to tumorigenesis and metastasis of ACC.
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