| Summary: | 碩士 === 國立中興大學 === 生物醫學研究所 === 98 === Phosphatase of regenerating liver 3 (PRL3) is a member of PRL protein tyrosine phosphatase family. Recent reports indicated that high level of PRL3 expression might be involved in colorectal cancers tumorigenesis and metastasis. In other cancers like breast carcinomas, gastric carcinomas and ovarian cancers, overexpression of PRL3 would similarly promote cell proliferation, migration and invasion. In recent years, lung cancer became one of the most serious cancers. In Taiwan, lung cancers also caused highly incidence rate and fatality rate. However, little is known about PRL3 function in lung cancer. In order to investigate the correlation between PRL3 and lung cancer, first we confirmed overexpression of PRL3 in SW480 would promote invasion, and overexpression of catalytic PRL3 mutant (C104S) effectively diminished the PRL-3-mediated invasion, as previous study. In lung cancer, we found that PRL3 expression in CL1-5, a highly invasive cell line, was lower than CL1-0, a lowly invasive cell line. Overexpression of PRL3 in CL1-5 remarkable inhibition capability of proliferation, migration, invasion, and colony formation compared with mock cells. Conversely, overexpression of catalytic PRL3 mutant (C104S) and PRL3 mutant (C170S) would enhance cell invasion. Furthermore, nude mice were subcutaneous injection with CL1-5 cells transfected with empty vector or c-myc-PRL3 vector. Twenty-eight days later, less tumorigenesis was found in mice injected with c-myc-PRL3 transfected cells than with mock cells. Finally, we surveyed gene expression between mock cells and PRL3-overexpression cells by microarray, and we focused on focal adhesion and related adhesion molecules via preliminary analysis possible pathway regulated by PRL3. Taken together, PRL3 might play a role of tumor suppressor in lung cancer, which is different from other cancers.
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