Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We are interested in the possibility of a new prostate cancer therapy that would control tumor malignancy via induction of terminal cell differentiation. We previously reported that 12-O-tetra-decanoylphorbol-13-acetate (TPA) induces differentiation into cells with characteristics of microglia and decreases the malignant characteristics of human prostatic cancer TSU-Pr1 cells. To investigate the mechanism underlying differentiation of TSU-Pr1 cells, we attempted to identify genes expressed during differentiation using differential display. We identified four genes expressed differentially after TPA treatment. Levels of expression of two genes, human flavoprotein subunit of complex II and JKTBP, were downregulated by TPA, and expression of two genes, human golgin p245 and bcl-xL, was upregulated. Moreover, we found that the changes in expression of flavo-protein, JKTBP and bcl-xL induced by TPA were blocked by treatment with protein kinase C (PKC) or mitogen-activated protein (MAP) kinase inhibitors that prevent TPA-induced differentiation of TSU-Pr1 cells. These results suggest that the differential expression of these genes is associated with TPA-induced differentiation of TSU-Pr1 cells. We expect that understanding the roles of these genes during differentiation will provide for new approaches and therapeutic targets for treatment of prostate cancer.
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PMID:Differential expression of genes during TPA-induced differentiation of human prostatic cancer TSU-Pr1 cells. 1243

Heterogenous nuclear ribonucleoprotein D-like protein (JKTBP) belongs to a new member of hnRNPs. Previous studies implied that JKTBP1 may be associated with the progression of androgen-independent (AI) prostate cancer. In this study, we generated three stable LNCaP cell lines which expressed exogenous JKTBP1. Furthermore, the effect of ectopic JKTBP1 on the proliferation of LNCaP cells and its mechanism was investigated. We originally found that the ectopic JKTBP1 expression resulted in the proliferation of LNCaP cells in an AI way, as well as inducing the upregulated expression of EGF-R and prostate-specific antigen (PSA), but did not influence the expression level of AR. Moreover, AG1478 suppressed the effect of proliferation induced by JKTBP1. In addition, immunohistochemistry showed that JKTBP1 expression was significantly elevated in AI prostate cancer tissues when compared with the androgen-dependent (AD) prostate cancer and benign prostatic hyperplasia. Our data indicated that overexpression of JKTBP1 in LNCaP cells leads to abnormal cell proliferation and may be involved in the process of AD to AI through induction of EGF-R expression.
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PMID:Overexpression of JKTBP1 induces androgen-independent LNCaP cell proliferation through activation of epidermal growth factor-receptor (EGF-R). 1838 62