| Prostate cancer is the most common malignant tumor and the second leading cancer death in men in the United States. Recent, along with the prolonging of the average life, the changing of life style and the proving of detecting way, the incidence and mortality of prostate cancer in many Asia countries have increased gradually than before, such as in China and Japan. most prostate cancers patients lost the potentially curable chance when they were diagnosed and ultimately developed hormone-refractory prostate cancer (HRPC) and dead of distribution of cancer cell. The incidence of prostate cancer has increased dramatically in the United State since the application of prostate specific antigen testing(PSA). The natural history of prostate cancer is poorly understood, but progression appears to be related to stage and grade of tumor, Biologically, prostate cancer represents a heterogenous disease entity that exhibits various degrees of aggressiveness, patterns of metastasis, and response to therapy. therefore, there is a great need to identify molecular prognositic factors that allow stratification of prostate cancer patients into homogeneous treatment groups. furthermore, the identification of new molecular targets may lead to more effective treatments for prostate cancer.STATs, signal transducers and activator of transcription , are latent cytoplasmic transcription factors that function as intracellular effectors of cytokine and growth factor signaling pathways. STAT proteins were originally defined in the context of normal cell signaling, where STATs have been implicated in control of cell proliferation, differentiation, and apoptosis. stat3, a member of STATs family, have been shown to play a key role in promoting proliferation, differentiation, anti-apoptosis or cell cycle progression. it transmit signals from cell surface receptors directly to the nucleus by binding directly to high affinity DNA binding sites or by associating with other transcription factors. There is evidence to implicate that stat3 is constitutively activated and overexpressed in a variety of tumours cell lines including leukemias, multiple myeloma, head and neck cancer, breast cancer, lung cancer.. This suggests that stat3 represents a promising molecular target for novel tumor therapy.Recent studies have indicated that inhibition of STAT3 activity in human tumor cells induces apoptosis and /or growth arrest in vitro. In human head and neck squamous carcinoma cells, interrupting stat3 signaling by antisense olignucleotides or decoy oligunucleotide abrogate transforming growth factor-α induced oncogenic growth of these cells .blocking stat3 signal by antisense induce human prostate cancer cells to apoptosis also ; stat3β is a dominant-negative stat3 variant, which is a truncated form of stat3 that contains the dimerization and DNA-binding domain but lacks the transactivation domain. As a consequence ,stat3β can bind DNA but cannot transactivate gene expression, thus blocking stat3 signaling in a trans-dominant negative fashion in most cases. Blocking stat3 signaling by stat3β in human myeloma cells down-regulates IL-6-induced expression of the antiapoptotic gene, Bcl-XL, resulting in a dramatic sensitization of cells to Fas-mediated apoptosis in vitro. Blocking stat3 activity by dominant-negative stat3βin breast cancer cells leads to apoptosis also .similar to multiple myeloma, disrupting stat3 signaling in head and neck cancer and prostate cancer cells inhibit BcL-XL expression and induces apoptosis. knockdown of stat3 expression by siRNA induces apoptosis in astrocytoma cells .these findings raise the possibility that targeting stat3 may result in antitumor responses in vivo in a wide variety of human cancers. RNA interference (RNAi) is the process of sequence-specific posttranscriptional gene silencing triggered by double-stranded RNAs(dsRNAs) homologous to the silenced gene . this phenomenon was first observed from studies in Caenorhabditis elegans and Drosophila melanogaster and was subsequently found i...
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