The product of transmembrane and coiled-coil domains 1 (TMCO1) gene is a member of several eukaryotic proteins with unknown function. In a preliminary Bioinformatics and Stanford Microarray Database data-mining and some of our preliminary data, transmembrane and coiled-coil domains 1 (TMCO1) immunohistochemistry (IHC) was identified to be up-regulated in non-invasive bladder cancer. To further studies on the functions and regulatory mechanisms the role of TMCO1 gene. In the present study, we examined the TMCO1 expression levels in human bladder cell lines, RT4, TSGH8301, J82. We observed TMCO1 high expression in RT4 and low expression in TSGH8301. We investigate overexpression and knock down of TMCO1in RT4 and TSGH8301. Further we study the expression change of TOMCO1 how to change cell function and morphology. In this study, we can get transfection of shRNA interference targeting TMCO1 in RT4 cell enhanced cell proliferation.

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Epithelial membrane protein 2(EMP2), a growth arrest specific-3/peripheral myelin protein-22(GAS3/PMP22) family member, is a tetraspan protein. In prior study identified EMP2 in endometrial cancer was an oncogene, but in B-cell lymphoma was a tumor suppressor gene. The effects of EMP2 on various cancer cell lines precise molecular mechanisms are not clear until now. We observed EMP2 was down-regulated following the progressive grades of bladder cancer cell lines. So, we clone the EMP2 full-length cDNA into the pEGFP-N3 vector as an tool. Then, we overexpressed EMP2 in bladder cancer cell line J82 cells and knockdown EMP2 by shEMP2 in bladder cancer cell line RT4 cells in order to examine its effects on functions of cells like proliferation, cycle , apoptosis and metastasis. Conclusion, we can get cell proliferation of EMP2-overexprssed cells were decreased through arresting G2/M phase of cell cycle. On the other hand, knockdown of EMP2 in RT4 cells increased cell proliferation. Moreover, the ability of migration were decreased by EMP2 in both J82 and RT4 cells.

Bladder cancer is the second most common genitourinary tumor and is a significant cause of morbidity and mortality. To find the noninvasive tumor marker for bladder cancer is still a challenge. Recently, the circulating cell-free DNA had been used for detection of some tumors. However, most of these studies selected the blood sample as the free DNA source. The purpose of this thesis is to develop and evaluate the more noninvasive method and tumor marker for bladder cancer detection, especially for the cell-free DNA. Three directions were addressed as followed: 1). urine cell-free DNA makers such as creatinine-adjusted cell-free DNA concentration, 2). DNA integrity (DNA length) and 3). Promoter hypermethylation for DNA repair genes. First, creatinine-adjusted urine cell-free DNA concentration was quantified via real time PCR. The real time PCR-based detection is based on detection large fragment cell-free DNA. Real time PCR-based urine cell-free DNA concentration of bladder cancer patients was higher than controls. Mean concentrations of 36 bladder cancer patients and 93 controls which detected by real time PCR were 14.98 and 1.07 pg/