Aim Through interfering the expression of survivin with short hairpin RNA(shRNA) technology,to investigate the effect of downregulation of survivin on cell apoptosis and chemosensitivity to docetaxel in breast cancer MCF-7 cells.Methods(1) Using MCF-7 cells as a model system,three groups were set up transfected with lipofectamine,RNAi control plasmid and survivin RNAi plasmid,respectively.The expression of survivin in MCF-7 cells was measured at transcriptional and translational level by using RT-PCR and Western blot methods.(2) The effect on the cell cycle and apoptosis was analyzed with flow cytometry.(3) The viability of cells applied with different doses of ducetaxel was determined by using the method of 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide reduction(MTT method).Results(1) RT-PCR and Western blot demonstrated that survivin expression was significantly decreased by transfection with RNAi targeting plasmid;the expression proportion was reduced by nearly 75.4% and 79.8%(P

Objective:To investigate the quality of life in children with McCune-Albright syndrome (MAS) and its influencing factors, so as to provide scientific basis for improving their quality of life.Methods:The clinical data of 31 children with MAS diagnosed (MAS group) and followed up in Henan Children′s Hospital from June 2015 to December 2021 were retrospectively analyzed.During the same period, 37 healthy age and sex-matched children at a ratio of 1∶1 were recruited as healthy control group.The children′s Quality of Life Universal Core Scale (PedsQL?4.0) was used for the investigation and comparative analysis.Statistical analysis was performed using the independent sample t test, Chi- square test and multiple regression analysis. Results:Compared with the healthy control group, the physiological function ( t=2.092, P<0.05), emotional function ( t=2.373, P<0.05) and total score ( t=2.360, P<0.05) of MAS group significantly decreased.Multiple regression analysis showed that physiological function was negatively correlated with the annual number of vaginal bleeding ( t=-2.367, P<0.05) and the age of first fracture ( t=-2.606, P<0.05). Social function was negatively correlated with the number of fractures ( t=-2.481, P<0.05). Conclusions:The overall quality of life of MAS children is low, especially the quality of physiological function and emotional function.The annual number of vaginal bleedings, the age of the first fracture and the number of fractures are influencing factors for the reduction of the quality of life of children with MAS.

OBJECTIVETo investigate the effects of long non-coding RNA(lncRNA) RP11-770J1.3 and transmembrane protein 25 (TMEM25) on paclitaxel resistance in human breast cancer MCF-7/PR cell line.

METHODSThe expression of lncRNA RP11-770J1.3 and TMEM25 in human breast cancer MCF-7(paclitaxel sensitive) and MCF-7/PR(paclitaxel resistant) cells were detected by quantitative RT-PCR. The synthetic interfering fragments of lncRNA RP11-770J1.3 and TMEM25 were transfected into MCF-7/PR cells. Sulforhodamine B assay was used to detect the sensitivity of MCF-7/PR cells to paclitaxel after interference of lncRNA RP11-770J1.3 and TMEM25. The expression of multidrug-resistance genes and proteins were detected by qRT-PCR and Western blot, respectively.

RESULTSlncRNA RP11-770J1.3 and TMEM25 were highly expressed in MCF-7/PR cells, and were significantly down-regulated after transfection of synthetic interfering fragments. Down-regulation of lncRNA RP11-770J1.3 and TMEM25 enhanced the sensitivity of MCF-7/PR cells to paclitaxel, and inhibited the expression of MRP, BCRP and MDR1/P-gp (all<0.05). Such effects were more significant when lncRNA RP11-770J1.3 and TMEM25 were both down-regulated (all<0.05).

CONCLUSIONSlncRNA RP11-770J1.3 and TMEM25 are highly expressed in MCF-7/PR cells, and the down-regulation of lncRNA RP11-770J1.3 and TMEM25 can enhance paclitaxel sensitivity in MCF-7/PR cells.

OBJECTIVETo investigate the effect of CXC chemokine receptor 4 (CXCR4) on cell cycle of breast cancer and its molecular mechanisms.

METHODSThe expression of CXCR4 and S phase kinase associated protein 2 (Skp2) was detected by real-time fluorescence quantitative PCR (fqRT-PCR) and Western blot in breast cancer cells. The expression of signal proteins and the downstream genes of Skp2 was detected by Western blot. The effect of CXCR4, PI3K/Akt pathway inhibitor LY294002 and ERK pathway inhibitor U0126 on cell cycle of breast cancer was detected by propidium iodide staining.

RESULTSSkp2 was significantly down-regulated in CXCR4-downregulated cells and up-regulated in CXCR4-upregulated cells. CXCR4 also regulated the expression of Skp2 and other downstream genes by signaling protein. The proportion of cells in G/Gphase increased and that in S phase declined in CXCR4-downregulated cell, and the effect was more significant when combined with the use of LY294002 or U0126.

CONCLUSIONSCXCR4 can affect cell cycle and inhibit the proliferation of breast cancer cells by regulating Skp2 gene expression through PI3K/Akt and ERK signaling pathway.