0.05). The positive rate of ER expression was lower in young age-group than in the other two groups,the differences among the three groups was statistically significant (P0.05). The rate of Her-2 expression was higher in young age-group than in both middle age-and elderly-group (P

Aiming at building research disciplines,Xijing hospital has initially achieved a strategic transformation into a hospital with research disciplines,with such measures as scientific layout of disciplines,making of advantageous disciplines with overseas benchmarks,encouragement of potential disciplines with advantageous disciplines,promotion of medical innovation with innovative ideas,and upgrading clinical service quality with technical innovation.

OBJECTIVETo study the effect of BRCA1 in regulating the proliferation and migration of breast cancer cells stimulated by progesterone.

METHODSBreast cancer MCF-7 and T-47D cell were transfected with a vector containing the coding sequence of BRCA1 (pFlag-CMV2-BRCA1 wt) to induce BRCA1 overexpression or with the empty vector (control). The cells were then stimulated with progesterone, and the cell proliferation and migration were observed using MTT assay and wound healing assay, respectively. The proliferation and migration of MCF-7 cells were also observed following transfection with a small interfering RNA (siRNA) for BRCA1 knockdown or with a scrambled siRNA prior to progesterone stimulation.

RESULTSTransfection with the empty vector and with pFlag-CMV2-BRCA1 wt prior to progesterone stimulation caused significantly different proliferation rates in MCF-7 cells [(114.4∓6.0)% vs (82.1∓3.2)%, P<0.05] and in T-47D cells [(111.3∓4.3)% vs (84.2∓3.5)%, P<0.05], resulting also in significantly different cell migration rates (55.9% vs 15.8% in MCF-7 cells and 44.83% vs 10.43% in T-47D cells). Compared to the scrambled siRNA, BRCA1 siRNA transfection prior to progesterone stimulation significantly increased the proliferation rates [(114.4∓3.05)% vs (125.3∓4.0)%, P<0.05] and migration rate (39.2% vs 69.08%) of MCF-7 cells. The progesterone antagonist RU468 could antagonize the effects of BRCA1 knockdown in enhancing progesterone-stimulated MCF-7 cell proliferation and migration.

CONCLUSIONA decreased BRCA1 expression can enhance progesterone-stimulated tumor cell proliferation and migration in sporadic breast cancer.

BRCA1 Protein ; metabolism ; Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Female ; Genetic Vectors ; Humans ; Progesterone ; pharmacology ; RNA, Messenger ; genetics ; Receptors, Progesterone ; antagonists & inhibitors ; Transfection

Objective To understand the spatial distribution characteristics of wild feces in schistosomiasis endemic areas of Jiangling County,Hubei Province and further explore the source of infection efficiently,so as to provide the evidence for the development of corresponding monitoring and response technology. Methods In 2011,the fresh wild feces were investigated every two months in the selected 15 villages by the severity of historical endemic in Jiangling County. The schistosome miracidi-um hatching method was used to test the schistosome infection of the wild feces. The descriptive analysis and spatial analysis were used for the description of the spatial distribution of the wild feces. Results Totally 701 wild feces samples were collected with the average density of 0.0556/100 m2,and the positive rate of the wild feces was 11.70%(82/701). The results of the re-gression analysis showed a positive spatial correlation between the positive rate of wild feces and the rate of human infection,the area with infected Oncomelania hupensis and the number of fenced cattle,and the corrected R2 of the model was 0.58. Conclu-sion The infection rate of wild feces is positively correlated with the rate of human infection,area with infected O. hupensis and number of fenced cattle in space in Jiangling County,so the prevention and control measures could be conducted according to the spatial distribution of the positive wild feces.

Objective To investigate the effect of tricostantin A (TSA) on self-renewal of breast cancer stem cells and explore the mechanisms. Methods Breast cancer cell lines MDA-MB-468, MDA-MB-231, MCF-7 and SKBR3 were cultured in suspension and treated with different concentrations of TSA for 7 days, using 0.1% DMSO as the control. Secondary mammosphere formation efficiency and percentage of CD44+/CD24-sub-population in the primary mammospheres were used to evaluate the effects of TSA on self-renewal of breast cancer stem cells. The breast cancer stem cell surface marker CD44+/CD24- and the percentage of apoptosis in the primary mammospheres were assayed using flow cytometry. The mRNA expressions of Nanog, Sox2 and Oct4 in the primary mammospheres were assayed with quantitative PCR. Results TSA at both 100 and 500 nmol/L, but not at 10 nmol/L, partially inhibited the self-renewal of breast cancer stem cells from the 4 cell lines. TSA at 500 nmol/L induced cell apoptosis in the primary mammospheres. TSA down-regulated the mRNA expression of Nanog and Sox2 in the primary mammospheres. Conclusions TSA can partially inhibit the self-renewal of breast cancer stem cells through a mechanism involving the down-regulation of Nanog and Sox2 expression, indicating the value of combined treatments with low-dose TSA and other anticancer drugs to achieve maximum inhibition of breast cancer stem cell self-renewal. The core transcriptional factor of embryonic stem cells Nanog and Sox2 can be potential targets of anticancer therapy.

Objective To investigate the effect of tricostantin A (TSA) on self-renewal of breast cancer stem cells and explore the mechanisms. Methods Breast cancer cell lines MDA-MB-468, MDA-MB-231, MCF-7 and SKBR3 were cultured in suspension and treated with different concentrations of TSA for 7 days, using 0.1% DMSO as the control. Secondary mammosphere formation efficiency and percentage of CD44+/CD24-sub-population in the primary mammospheres were used to evaluate the effects of TSA on self-renewal of breast cancer stem cells. The breast cancer stem cell surface marker CD44+/CD24- and the percentage of apoptosis in the primary mammospheres were assayed using flow cytometry. The mRNA expressions of Nanog, Sox2 and Oct4 in the primary mammospheres were assayed with quantitative PCR. Results TSA at both 100 and 500 nmol/L, but not at 10 nmol/L, partially inhibited the self-renewal of breast cancer stem cells from the 4 cell lines. TSA at 500 nmol/L induced cell apoptosis in the primary mammospheres. TSA down-regulated the mRNA expression of Nanog and Sox2 in the primary mammospheres. Conclusions TSA can partially inhibit the self-renewal of breast cancer stem cells through a mechanism involving the down-regulation of Nanog and Sox2 expression, indicating the value of combined treatments with low-dose TSA and other anticancer drugs to achieve maximum inhibition of breast cancer stem cell self-renewal. The core transcriptional factor of embryonic stem cells Nanog and Sox2 can be potential targets of anticancer therapy.