A Proteomic Analysis of Tumorigenic and Non-Tumorigenic Cells from the Prostate Carcinoma Cell-line DU145
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Abstract A small population of cells with stem cell‐like properties in prostate cancer ( PC a), called prostate cancer stem cells (Pr CSC s) or prostate stemness‐high cancer cells, displays highly tumorigenic and metastatic features and may be responsible for the therapy resistance. A small molecule, napabucasin ( BBI 608), recently have been identified with suppression of stemness‐high cancer cells in a variety of cancers. However, the effects of napabucasin on PC a cells as well as Pr CSC s isolated from PC a cells have not yet been defined. The effect of napabucasin on PC a cells in cell proliferation, colony formation, and cell migration in vitro were measured by MTS , colony formation assay, and Transwell, respectively. Flow cytometry was employed to evaluate cell cycle and cell apoptosis, and the effect on tumorigenesis in vivo was examined by tumor growth assays. Furthermore, the role of napabucasin on self‐renewal and survival of Pr CSC s was evaluated by their ability to grow spheres and cell viability assay, respectively. Western Blot and qRT ‐ PCR were used to determine the effect of napabucasin on the expressions of stemness markers. Decrease in cell viability, colony formation, migration, and survival with cell cycle arrest, higher sensitivity to docetaxel in vitro, and repressed tumorigenesis in vivo was observed upon napabucasin treatment. More importantly, napabucasin can obviously inhibit spherogenesis and even kill Pr CSC s in vitro. Downregulation of stemness markers was observed after Pr CSC s were treated with napabucasin. This study demonstrates that napabucasin may be a novel approach in the treatment of advanced PC a, specifically for castration‐resistant prostate cancer ( CRPC ).
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We have taken the following strategy to investigate the role of oncogenes in the neoplastic transformation of human bronchial epithelial cells. First, activated protooncogenes that are associated with human lung cancer are identified. Next, these oncogenes are transferred into the progenitor epithelial cells of broncheogenic carcinoma. The preneoplastic and neoplastic cells are then selected out from the putative suppressive normal cells. The tumorigenicity of the cells containing the transfected oncogenes is then determined using the athymic nude mouse assay system. If the transfected or infected cells show increased tumorigenicity, the dysregulation in the molecular controls of growth and terminal differentiation are then investigated. The methods used to investigate tumor suppressor genes involves several different methodologies including production of somatic cell-cell hybrids with tumorigenic and non-tumorigenic cells, and analysis of mutational events in known tumor suppressor genes in human lung carcinoma cell lines and tumors.
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The human galectin-3 is a galactoside-binding protein of 31 kDa which functions as a receptor for glycoproteins containing poly N-acetyllactosamine side chains and as a substrate for matrix metalloproteinases-2 and -9. We studied its expression by flow cytoflourimetry, Western, Northern and Southern analyses, in five cultured human breast carcinoma cell lines previously characterized as nontumorigenic, poorly metastatic or metastatic in nude mice. The expression of galectin-3 correlated with the reported tumorigenicity of the cells. The introduction of recombinant galectin-3 into the null expressing non-tumorigenic BT-549 cells resulted in the acquisition of anchorage-independent growth properties in all and tumorigenicity in 3/4 sense transfected cell clones. The data indicate a relationship between galectin-3 expression and malignancy of human breast carcinoma cell lines.
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