Objective To study expression of NDRG3 in prostatic mesenchyma and effect of exogenous NDRG3 on prostatic stromal cells. Methods Immunohistochemical analysis was used to check expression of NDRG3 in prostate mesnenchy...Objective To study expression of NDRG3 in prostatic mesenchyma and effect of exogenous NDRG3 on prostatic stromal cells. Methods Immunohistochemical analysis was used to check expression of NDRG3 in prostate mesnenchyma. The WPMY-1 prostate immortalized mesenchyma cell line was stably-transfected with a NDRG3 gene expression vector. The NDRG3-stable transfected WPMY-1 sublines were studied along with parental and empty vector transfected WPMY-1 cells as controls. RT-PCR technology was applied to identity downstream gene expression under regulation of NDRG3 expression.Results Expression of DNRG3 was observed in prostate cancer mesenchyma, over-expression of NDRG3 in WPMY-1 cell up-regulated expression of chemotatic factors-CXCL3 and CXCL5. Conclusion Expression of stromal NDRG3 in prostate cancer specimens is significantly higher than that in benign prostatic hypertrophy （BPH） sample. There is a remarkable difference between the two groups of samples, NDRG3 may be related to angiogenesis in prostatic mesenchyma.展开更多
Objective To investigate the miR-296＇s function in prostate carcinoma（PCa） cells. Methods In order to profile the miRNA expression in LNCaP cells, the cultured cells were stimulated with androgen after 48-h starvat...Objective To investigate the miR-296＇s function in prostate carcinoma（PCa） cells. Methods In order to profile the miRNA expression in LNCaP cells, the cultured cells were stimulated with androgen after 48-h starvation, miRNA microarray analysis and Q-RT-PCR assay were performed. To characterize the effects of miR296 on PCa cells, CL-1 and PC-3 cells were transfected with miR-296 and antisense-miR-296, cell growth and apoptosis were then analyzed. Results The miR-296-5p expression was up-regulated by 2.22 folds in the CL-1 cells, which do not express significantly androgen receptor, than in LNCaP cells. Knockdown of miR-296-5p induced apoptosis of CL-1 cells, but not LNCaP cells. However, knockdown of miR-296-5p inhibited the growth rate of LNCaP cells cultured in absence of androgen. Conclusion MiR-296-5p could be important for development of prostate cancer from androgen dependence to androgen independence.展开更多
OCT4, a member of the POU family of gene products, is an octamer motif-binding transcription factor. As it is known to play a crucial role in cancer processes including proliferation, invasion, and chemoradioresistanc...OCT4, a member of the POU family of gene products, is an octamer motif-binding transcription factor. As it is known to play a crucial role in cancer processes including proliferation, invasion, and chemoradioresistance, it is important to identify the direct targets of OCT4 in living cancer cells. Here, chromatin immunoprecipitation-sequencing （ChlP-seq） was used to identify OCT4 binding sites in glioblastoma cancer cells. The results showed that 5438 OCT4 binding sites were localized in the glioblastoma cancer genome and that these sites contained a consensus sequence TTTkswTw （k=T or G, s=C or G, w=A or T）, which occurred 3931 times in 2312 OCT4 binding regions. Furthermore, binding motifs of some other transcription factors were identified in OCT4 binding regions. Our results provide a valuable dataset for understanding gene regulation mechanisms underlying the function of OCT4 in glioblastoma cancer.展开更多
基金Shanghai Municipal Committee of Science and Technology (06ZR14072)
文摘Objective To study expression of NDRG3 in prostatic mesenchyma and effect of exogenous NDRG3 on prostatic stromal cells. Methods Immunohistochemical analysis was used to check expression of NDRG3 in prostate mesnenchyma. The WPMY-1 prostate immortalized mesenchyma cell line was stably-transfected with a NDRG3 gene expression vector. The NDRG3-stable transfected WPMY-1 sublines were studied along with parental and empty vector transfected WPMY-1 cells as controls. RT-PCR technology was applied to identity downstream gene expression under regulation of NDRG3 expression.Results Expression of DNRG3 was observed in prostate cancer mesenchyma, over-expression of NDRG3 in WPMY-1 cell up-regulated expression of chemotatic factors-CXCL3 and CXCL5. Conclusion Expression of stromal NDRG3 in prostate cancer specimens is significantly higher than that in benign prostatic hypertrophy （BPH） sample. There is a remarkable difference between the two groups of samples, NDRG3 may be related to angiogenesis in prostatic mesenchyma.
文摘Objective To investigate the miR-296＇s function in prostate carcinoma（PCa） cells. Methods In order to profile the miRNA expression in LNCaP cells, the cultured cells were stimulated with androgen after 48-h starvation, miRNA microarray analysis and Q-RT-PCR assay were performed. To characterize the effects of miR296 on PCa cells, CL-1 and PC-3 cells were transfected with miR-296 and antisense-miR-296, cell growth and apoptosis were then analyzed. Results The miR-296-5p expression was up-regulated by 2.22 folds in the CL-1 cells, which do not express significantly androgen receptor, than in LNCaP cells. Knockdown of miR-296-5p induced apoptosis of CL-1 cells, but not LNCaP cells. However, knockdown of miR-296-5p inhibited the growth rate of LNCaP cells cultured in absence of androgen. Conclusion MiR-296-5p could be important for development of prostate cancer from androgen dependence to androgen independence.
基金supported by the Ministry of Science and Technology, China(Nos. 2004CB518707, 2006DFA32950, 2006AA02Z4A2, 2006AA02A303, 2007DFC30360, and 2008DFA11320)the National Natural Science Foundation of China (No. 81101580)
文摘OCT4, a member of the POU family of gene products, is an octamer motif-binding transcription factor. As it is known to play a crucial role in cancer processes including proliferation, invasion, and chemoradioresistance, it is important to identify the direct targets of OCT4 in living cancer cells. Here, chromatin immunoprecipitation-sequencing （ChlP-seq） was used to identify OCT4 binding sites in glioblastoma cancer cells. The results showed that 5438 OCT4 binding sites were localized in the glioblastoma cancer genome and that these sites contained a consensus sequence TTTkswTw （k=T or G, s=C or G, w=A or T）, which occurred 3931 times in 2312 OCT4 binding regions. Furthermore, binding motifs of some other transcription factors were identified in OCT4 binding regions. Our results provide a valuable dataset for understanding gene regulation mechanisms underlying the function of OCT4 in glioblastoma cancer.
