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Objective:To explore the mechanism by which microRNA (miRNA) -1303 inhibits the proliferation and migration of renal cell carcinoma 786-O cells through targeted regulation of lysophosphatidic acid receptor 3 (LPAR3) expression.Methods:quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative expression of miR-1303 in renal cancer cell lines (A498, ACHN, 786-O, OS-RC-2) and normal renal tubular epithelial cells HK-2. The miR-1303 mimic and the negative control sequence were transfected into the renal cancer cells with the lowest expression of miR-1303, respectively, as the miR-1303 group and the negative control group. qRT-PCR detected the relative expression of miR-1303 in the two groups of cells. MTT method and Transwell migration experiment were used to detect cell proliferation and migration ability. RegRNA 2.0 predicted the target genes of miR-1303. The dual luciferase reporter gene detected the binding of miR-1303 to the target gene. qRT-PCR and Western blotting detected the relative expression of LPAR3. Measurement data were expressed as mean±standard deviation ( ± s), t-test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:The expressions of miR-1303 in renal cancer cell lines A498, ACHN, 786-O, OS-RC-2 and normal renal tubular epithelial cells HK-2 were 0.51±0.04, 0.79±0.02, 0.21±0.04, 0.55±0.07 and 1.00±0.05, the expression of miR-1303 in renal cancer cell lines was lower than that in HK-2 ( P<0.05), and the relative expression in 786-O cells was the lowest ( F=29.50, P<0.01). Compared with the control group, the expression of miR-1303 in the experimental group was significantly increased [(1.00±0.01) vs (7.98±0.88), t=7.95, P<0.01]. The cell absorbance value of the experimental group was significantly lower than that of the control group ( P<0.05). The number of cell migration in the experimental group was significantly lower than that in the control group ( P<0.05). miR-1303 can bind to LPAR3 mRNA in a complementary pair ( P<0.01). Compared with the control group, the expression of LPAR3 mRNA in the 786-O cells of the experimental group was significantly reduced [(1.00±0.01) vs (0.23±0.03), t=23.56, P<0.01]. Conclusion:miR-1303 may inhibit the proliferation and migration ability of renal cancer 786-O cells by down-regulating the expression of LPAR3.
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Objective:To investigate the effects of miR-5011-5p on apoptosis and migration of bladder cancer cell line J82 and the underlying mechanism.Methods:J82 cells were transfected with random sequence molecules (NC group) and miR-5011-5p sequence molecules (miR-5011-5p group). Flow cytometry and scratch experiment were performed to analyze the effects of miR-5011-5p on apoptosis and migration of J82 cells. The target gene of miR-5011-5p was predicted by bioinformatics. Real-time fluorescent quantitative polymerase chain reaction and western blot assay were performed to investigate the effects of miR-5011-5p on target gene expression.Results:The relative expression of miR-5011-5p in J82 cells in the miR-5011-5p group was significantly higher than that in the NC group (10.73 ± 1.67 vs. 1.04 ± 0.16, t = 5.81, P < 0.01). There was significant difference in the apoptosis rate of J82 cells between NC and miR-5011-5p groups [(8.83 ± 1.67)% vs. (34.96 ± 3.80)%, t = 6.30, P < 0.01]. The migration rate of J82 cells differed significantly between NC and miR-5011-5p groups [(71.31 ± 7.69)% vs. (37.43 ± 5.01)%, t = 3.69, P < 0.05]. The target gene of miR-5011-5p may be Yes-related protein 1 (YAP1). Compared with the NC group, miR-5011-5p exhibited an obvious inhibitory effect on the YAP1 expression in J82 cells ( P < 0.01). Conclusion:miR-5011-5p may promote the apoptosis of J82 cells and inhibit their migration in bladder cancer through targeted inhibition of YAP1 gene expression.
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Objective:To observe the expression of microRNA (miRNA, miR) -7850 in renal cancer tissues, and to explore the effect of miR-7850 on the proliferation and migration of renal cancer cells and on the regulation of serine proteinase inhibitor B3 (SERPINB3) gene expression.Methods:Real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-7850 in renal cancer tissues and renal cancer cell lines. The renal cell carcinoma cell line with the lowest expression of miR-7850 was selected, and the negative control sequence (miR-NC) and miR-7850 mimics were transfected into renal cell carcinoma cells by Lipofectamine 2000 transfection reagent, respectively, which were defined as miR-NC group and miR-7850 group. qRT-PCR was used to detect the expression of miR-7850 in transfected renal cancer cells. The cell proliferation and migration ability after transfection were detected by cell counting kit-8 (CCK-8) method and transwell experiment. Bioinformatics prediction and dual luciferase reporter gene experiments were used to verify the target gene of miR-7850. qRT-PCR and Western blot were used to detect the expression of target genes in renal cancer cells after transfection.Results:Compared with adjacent tissues (5.95±0.44), the expression of miR-7850 in kidney cancer tissues (1.19±0.33) was lower ( P<0.01). Compared with immortalized proximal renal tubular epithelial cells (1.01±0.07), the expression of miR-7850 was lower in renal cancer cell lines ( P<0.05), and the lowest in A498 cells (0.13±0.01) ( P<0.01). The expression of miR-7850 in the miR-7850 group (7.46±0.93) was significantly higher than that in the miR-NC group (1.01±0.08) ( P<0.01), indicating successful transfection. Compared with the miR-NC group, the cell proliferation ability of the miR-7850 group was significantly reduced ( P<0.05). The number of migrating cells in miR-NC group and miR-7850 group were (139.50±12.31) and (75.09±16.05) cells, respectively, and the cell migration ability in miR-7850 group decreased significantly ( P<0.01). Bioinformatics technology shows that the target gene of miR-7850 was SERPINB3. The dual luciferase reporter gene experiment confirmed that miR-7850 can target the SERPINB3 gene ( P<0.05). Compared with the miR-NC group, the expression of SERPINB3 in cells of miR-7850 group was significantly reduced ( P<0.05), as well as the CDK4, CyclinD, Snail and Vimentin. Conclusions:miR-7850 is lowly expressed in renal cancer tissues and cell lines. miR-7850 can inhibit the proliferation and migration of renal cancer A498 cells, which may be related to its inhibition of SERPINB3 gene expression.
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Objective:To analyze the expression of long non-coding RNA (lncRNA) ZFPM2-AS1 in bladder cancer tissues and cell lines, and to observe the effect of down-regulating ZFPM2-AS1 on the migration and proliferation of bladder cancer cells and explore its molecular mechanism.Methods:Real-time quantitative fluorescent polymerase chain reaction (qRT-PCR) was used to detect the expression of ZFPM2-AS1 in 51 pairs of bladder cancer tissues and adjacent tissues, bladder cancer cell lines (J82, 5637, BIU-87, T24) and human normal bladder epithelial cells SV-HUC-1. The bladder cancer cells with the highest ZFPM2-AS1 expression were selected and transfected with the small interfering siRNA-ZFPM2-AS1 plasmid and the negative control plasmid, respectively, and defined as the experimental group and the control group. qRT-PCR was used to detect the expression of ZFPM2-AS1 in two groups of cells. Transwell migration test and tetramethylazozole blue (MTT) method were used to detect the cell migration ability and proliferation ability of the two groups. qRT-PCR was used to detect the expression of Up-frameshift mutant 1 (UPF1) mRNA in two groups of cells. Western blot was used to detect the expression of UPF1 and mTOR signaling pathway proteins in the two groups of cells.Results:The expression of ZFPM2-AS1 in bladder cancer tissues was significantly higher than that in adjacent tissues ( P<0.01). The expression of ZFPM2-AS1 in bladder cancer cell lines was significantly higher than that in human normal bladder epithelial cells ( P<0.01), and ZFPM2-AS1 had the highest expression in BIU-87 cells ( P<0.01). Compared with the control group, the expression of ZFPM2-AS1 in BIU-87 cells in the experimental group was significantly reduced [(1.01±0.06) vs (0.16±0.04), t=12.28, P<0.01]. Compared with the control group, the migration ability of BIU-87 cells in the experimental group was decreased ( P<0.05), and the proliferation ability of BIU-87 cells was significantly decreased from the second day ( P<0.05). Compared with the control group, UPF1 mRNA expression in BIU-87 cells in the experimental group was significantly decreased [(1.00±0.02) vs (0.28±0.04), t=15.49, P<0.01]. Western blot results showed that UPF1 protein expression and mammalian rapamycin target protein (mTOR), GRB2, IRS1 and p-PI3K signal pathway protein expression were decreased in BIU-87 cells. Conclusions:ZFPM2-AS1 is highly expressed in bladder cancer tissues and cell lines. Down-regulating ZFPM2-AS1 can inhibit the migration and proliferation of BIU-87 cells. The molecular mechanism may be related to the inhibition of UPF1 gene expression.
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Objective:To observe the expression of long non-coding RNA (lncRNA) PEBP1P2 in renal cell carcinoma (RCC) tissues and its effect on the proliferation and migration of RCC cells.Methods:The expression of PEBP1P2 in 51 RCC tissues and RCC cell lines was detected by real-time quantitative polymerase chain reaction (qPCR). The A498 cells with the lowest expression of PEBP1P2 were transfected, and the cells transfected with PEBP1P2 plasmid were used as the PEBP1P2 group, and the cells transfected with the negative control plasmid were used as the NC group. qPCR was used to detect the expression of PEBP1P2 in the two groups of cells. MTT assay and Transwell migration assay were used to detect the proliferation and migration ability of RCC cells. qPCR and Western blotting were used to detect the expression of caspase recruitment domain family member 10 ( CARD10) gene and NF-κB pathway protein, respectively. Measurement data were expressed as mean±standard deviation ( Mean± SD), and LSD- t test was used for comparison between groups. Results:The expression of PEBP1P2 in RCC tissues was lower than that in adjacent tissues ( t=4.89, P<0.01). The expression of PEBP1P2 in RCC cells was lower than that in normal renal tubular epithelial cells ( P<0.01). The expression of PEBP1P2 in A498 cells of the PEBP1P2 group and NC group was (11.01±1.26) and (1.06±0.19), respectively, and the PEBP1P2 group was significantly higher than that in the NC group ( t=7.81, P<0.01). Overexpression of PEBP1P2 significantly inhibited the proliferation of RCC cells ( P<0.05) and migration ability ( t=3.65, P<0.05). Overexpression of PEBP1P2 significantly suppressed the expression of CARD10 gene in RCC A498 cells ( t=6.83, P<0.01) and inhibited the transduction of NF-κB signaling pathway proteins. Conclusions:PEBP1P2 expression was significantly decreased in RCC tissues. Overexpression of PEBP1P2 significantly inhibited the proliferation and migration of RCC A498 cells. Its molecular mechanism is that PEBP1P2 down-regulates CARD10 gene expression and inhibits NF-κB signaling pathway.
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On the basis of real-world clinical data, the study aimed to explore the effect and mechanisms of the treatment plan of "traditional Chinese medicine (TCM) regulating liver regeneration." A total of 457 patients with HBV-related liver failure were retrospectively collected. The patients were divided into three groups: the modern medicine control group (MMC group), patients treated with routine medical treatment; the control group combining traditional Chinese and Western medicine (CTW), patients treated with routine medical treatment plus the common TCM formula; and the treatment group of "TCM regulating liver regeneration" (RLR), patients treated with both routine medical treatment and the special TCM formula of RLR. After 8 weeks of treatment, the mortality of patients in the RLR group (12.31%) was significantly lower than those in the MMC (50%) and CTW (29.11%) groups. Total bilirubin level significantly decreased and albumin increased in the RLR group when compared with the MMC and CTW groups (P < 0.05). In addition, there were significant differences in the expression of several cytokines related to liver regeneration in the RLR group compared with the MMC group. RLR treatment can decrease jaundice, improve liver function, and significantly reduce the mortality in patients with HBV-related liver failure. The mechanism may be related to the role of RLR treatment in influencing cytokines related to liver regeneration.
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Humanos , Medicamentos de Ervas Chinesas/uso terapêutico , Hepatite B/tratamento farmacológico , Falência Hepática , Regeneração Hepática , Medicina Tradicional Chinesa , Estudos RetrospectivosRESUMO
Objective To investigate the effect of long-chain non-coding RNA AL117378.1 on the proliferation and invasion of bladder cancer cells.Methods From August 2016 to December 2017,the tumor tissues and adjacent tissues of 14 patients with bladder cancer treated by Huangshi Central Hospital of Edong Healthcare Group were selected.Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of AL117378.1 in 14 pairs of bladder cancer tissues and corresponding adjacent tissues,bladder cancer cell lines (5637,J82,T24,BIU-87) and corresponding human bladder normal epithelial cells (SV-HUC-1).The negative control plasmid (control group) and the plasmid carrying the AL117378.1 (experimental group) were transfected into the bladder cancer cell line with the lowest expression level.qRT-PCR was used to detect the expression levels of ALl 17378.1 and non-receptor protein tyrosine phosphatase 9 (PTPN9)mRNA in the transfected cells.The expression levels of PTPN9,E-cadherin,o-SMA,CDK4 and Cyclin A2 protein were detected by Western blotting.MTT assay and Transwell invasion assay were used to detect the cell proliferative capacity and invasive ability of the two groups.Measurement data were expressed as mean ± standard deviation(Mean ± SD),and comparison between groups used independent sample t test.Results The expression of AL117378.1 in bladder cancer tissues was lower than that in adjacent tissues (P ＜ 0.01).The expression of AL117378.1 in bladder cancer cell lines was lower than that in human bladder normal epithelial cells (P ＜ 0.01),and the expression level of AL117378.1 was the lowest in J82 cells (P ＜ 0.01).The expression levels of AL117378.1 in the control and experimental groups were 1.02 ± 0.11 and 7.96 ± 1.06,respectively,and the difference was statistically significant (t =6.51,P ＜0.01).The expression of PTPN9 mRNA was 1.01 ± 0.08 and 4.99 ± 0.50,respectively.the difference was statistically significant (t =7.84,P ＜0.01).Western blotting results showed that the expression of PTPN9 and E-cadherin increased,and the expression of α-SMA,CDK4 and Cyclin A2 decreased.MTT experiments showed that the proliferation of cells transfected with AL117378.1 was significantly decreased (P ＜ 0.05).Transwell invasion experiments showed that the number of invasive cells in the control group and the experimental group were 97.96 ± 13.71 and 38.02 ±7.51,respectively,and the difference was statistically significant (t =3.84,P ＜ 0.01).Conclusions The expression of AL117378.1 was significantly decreased in bladder cancer tissues and cell lines (5637,J82,T24,BIU-87).ALl 17378.1 can significantly inhibit the proliferation and invasion of bladder cancer cells by positively regulating the expression of PTPN9 gene.
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Objective@#To investigate the effect of long-chain non-coding RNA AL117378.1 on the proliferation and invasion of bladder cancer cells.@*Methods@#From August 2016 to December 2017, the tumor tissues and adjacent tissues of 14 patients with bladder cancer treated by Huangshi Central Hospital of Edong Healthcare Group were selected. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of AL117378.1 in 14 pairs of bladder cancer tissues and corresponding adjacent tissues, bladder cancer cell lines (5637, J82, T24, BIU-87) and corresponding human bladder normal epithelial cells (SV-HUC-1). The negative control plasmid (control group) and the plasmid carrying the AL117378.1 (experimental group) were transfected into the bladder cancer cell line with the lowest expression level. qRT-PCR was used to detect the expression levels of AL117378.1 and non-receptor protein tyrosine phosphatase 9 (PTPN9) mRNA in the transfected cells. The expression levels of PTPN9, E-cadherin, α-SMA, CDK4 and Cyclin A2 protein were detected by Western blotting. MTT assay and Transwell invasion assay were used to detect the cell proliferative capacity and invasive ability of the two groups. Measurement data were expressed as mean± standard deviation(Mean±SD), and comparison between groups used independent sample t test.@*Results@#The expression of AL117378.1 in bladder cancer tissues was lower than that in adjacent tissues (P<0.01). The expression of AL117378.1 in bladder cancer cell lines was lower than that in human bladder normal epithelial cells (P<0.01), and the expression level of AL117378.1 was the lowest in J82 cells (P<0.01). The expression levels of AL117378.1 in the control and experimental groups were 1.02 ± 0.11 and 7.96 ± 1.06, respectively, and the difference was statistically significant (t=6.51, P<0.01). The expression of PTPN9 mRNA was 1.01 ± 0.08 and 4.99 ± 0.50, respectively. the difference was statistically significant (t=7.84, P<0.01). Western blotting results showed that the expression of PTPN9 and E-cadherin increased, and the expression of α-SMA, CDK4 and Cyclin A2 decreased. MTT experiments showed that the proliferation of cells transfected with AL117378.1 was significantly decreased (P<0.05). Transwell invasion experiments showed that the number of invasive cells in the control group and the experimental group were 97.96±13.71 and 38.02±7.51, respectively, and the difference was statistically significant (t=3.84, P<0.01).@*Conclusions@#The expression of AL117378.1 was significantly decreased in bladder cancer tissues and cell lines (5637, J82, T24, BIU-87). AL117378.1 can significantly inhibit the proliferation and invasion of bladder cancer cells by positively regulating the expression of PTPN9 gene.
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Objective To investigate the activation effect of microRNA-1280 (miR-1280) on the expression of p21 gene in bladder cancer cell line BIU-87 and its effect on cell cycle and proliferation of bladder cancer cell line.Methods Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the expressions of miR-1280 in bladder cancer cell lines T24,5637,J82,BIU-87 and normal bladder epithelial cells SV-HUC-1.miR-1280 mimics (experimental group) and miR-NC (control group) were transfected into the bladder cancer cells with the lowest expression of miR-1280.The expressions of miR-1280 and p21 mRNA were detected by qRT-PCR.Chromatin immunoprecipitation (ChIP) was used to verify the targeting effect of miR-1280 and p21 gene promoter.Western blotting was used to detect the expressions of p21,cell cycle-dependent kinase 1 (CDK1),Cyclin A2 mRNA and protein in the two groups.Cell cycle was detected by flow cytometry,and cell proliferation was detected by methyl thiazolyl tetrazclium (MTT) assay.Results The results of qRT-PCR indicated that the expression levels of miR-1280 in bladder cancer cell lines T24,5637,J82 and BIU-87 and normal urothelium cell line SV-HUC-1 were 0.503 ±0.094,0.611 ±0.054,0.567 ± 0.077,0.257 ± 0.032 and 1.014 ± 0.090 respectively,with a significant difference (F =1.880,P ＜0.001).Compared with bladder cancer cell lines T24,5637 and J82 cells,the expression of miR-1280 in BIU-87 cell was the lowest (P =0.026,P =0.003,P =0.008).Compared with the control group,the expression of miR-1280 in BIU-87 cell was significantly increased (1 041.000 ± 157.500 vs.1.023 ± 0.118,t =6.606,P ＜0.001),and the expression of p21 mRNA was also significantly increased (5.280 ± 0.660 vs.1.007 ± 0.070,t =6.440,P ＜ 0.001).Western blotting showed that p21 protein expression was up-regulated,CDK1 and Cyclin A2 protein expressions were down-regulated.ChIP experiments showed that compared with the miR-NC transfection group,the concentration of biotin modified miR-1280 in the p21 gene promoter region was significantly increased (1.246 ±0.171 vs.0.519 ± 0.087,t =3.787,P =0.009).The proportion of G0-G1 cells in the experimental group BIU-87 cells was significantly higher than that in the control group (68.360％ ±3.064％ vs.46.970％ ±3.971％,t =4.263,P =0.005).The results of MTT showed that compared with the control group,the cell proliferation ability of BIU-87 cells after being transfected miR-1280 was significantly decreased starting from day 3 (0.826 ± 0.099 vs.1.224 ± 0.057,t =3.505,P =0.013).Conclusion miR-1280 can activate the expression of p21 gene in bladder cancer cell line BIU-87 by binding the promoter region of p21 gene,blocking the progression of cell cycle and inhibiting cell proliferation,which provides a new direction for bladder cancer targeted therapy theory.
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Objective To investigate the effects of microRNA-1291 (miR-1291) on the expression of Zinc finger protein 8 (PHF8) gene in renal cell carcinoma and its effect on cell cycle and proliferation of renal cell carcinoma.Methods Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-1291 in renal cell carcinoma cell lines OS-RC-2,ACHN,A498,786-O and human proximal tubular epithelial cells HK-2.miR-1291 (miR-1291 group) and miR-NC (miR-NC group) were transfected into the renal cell lines with the lowest expression of miR-1291.qRT-PCR was used to detect the expression of miR-1291 and PHF8 mRNA in the transfected cells.The expression levels of PHF8,Cyclin-dependent kinase 6 (CDK6) and Cyclin D1 were detected by Western blotting.The effect of miR-1291 on the transcriptional activity of PHF8 was detected by double luciferase reporter gene system.Flow cytometry was used to detect cell cycle distribution.Methyl thiazolyl tetrazolium (MTT) assay and colony formation assay were used to detect cell viability and proliferation.Results The expressions of miR-1291 in renal carcinoma cell lines OS-RC-2,ACHN,A498,786-O and human proximal renal tubular epithelial cell HK-2 were 0.64 ± 0.17,0.60 ±0.15,0.29 ±0.08,0.63 ±0.08 and 1.01 ±0.17 respectively,with a significant difference (F=13.790,P ＜ 0.001).Compared with renal carcinoma cell lines OS-RC-2,ACHN and 786-O,the expression level of miR-1291 in A498 cell line was the lowest (P =0.002,P =0.006,P =0.003).The expression levels of miR-1291 in A498 cell lines of miR-NC group and miR-1291 group were 1.00 ± 0.03 and 775.25 ± 329.91 respectively,with a significant difference (t =4.694,P =0.003);and the expression levels of PHF8 mRNA were 1.00 ±0.11 and 0.57 ±0.18 respectively,with a significant difference (t =4.122,P =0.006).The results of Western blotting were consistent with the results of qRT-PCR,and the expressions of CDK6 and Cyclin D1 were significantly decreased.The double luciferase reporter gene showed that miR-1291could directly inhibit the activity of luciferase in the 3'un-translated region of target gene PHF8.Compared with miR-NC group,the proportion of renal carcinoma cells in S phase (23.40 ± 4.29 vs.32.19 ± 2.64;t =3.491,P =0.013) and G2-M phase (14.38 ± 4.05 vs.25.59 ± 6.01;t =3.095,P =0.021) decreased;and the proportion of cells in G0-G1 phase increased (62.22 ± 7.56 vs.42.22 ± 5.23,t =4.351,P =0.005).MTT assay showed that the cell viability of miR-1291 was significantly decreased.Colony formation experiments showed that the numbers of colonies formed by A498 cells in miR-NC group and miR-1291 group were 246.64 ± 39.94 and 87.34 ± 21.93 respectively,with a significant difference (t =6.993,P ＜ 0.001).Conclusion The expression of miR-1291 is significantly decreased in renal cancer cell lines.miR-1291 can significantly inhibit the proliferation of renal cell carcinoma cells by targeting interfering PHF8 gene expression,which may contribute to the development of new renal cancer target.
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Objective To investigate the effect of miR-103b on the expression of P21 protein in renal cell carcinoma cell line 769-P and ACHN cells,and its effect on the growth of renal cell carcinoma.Methods Renal cancer cells were divided into two groups according to the transfected RNA,miR-103b (experimental group) and dsControl (control group),respectively.Real-time PCR and Western blotting were used to detect the expression of P21,cell cycle-dependent kinase 6,Cyclin D1 mRNA and protein expression.Flow cytometry was used to detect the cell cycle distribution.MTT assay was used to detect cell viability and colony formation assay was used to detect cell proliferation.Measurement data were represented as x ± s.Comparison between groups was analyed using t test.Results Real-time PCR results showed that the relative expression levels of P21,cell cycle-dependent kinase 6 and Cyclin D1 mRNA in 769-P and ACHN which belong to control group cells were 1.00 ±0.10 and 1.02 ±0.27,1.00 ±0.08 and 1.01 ±0.17,1.01 ±0.19 and 1.00 ±0.02.The experimental group was 2.36 ±0.51 and 2.03 ± 0.49,0.33 ± 0.20 and 0.58 ± 0.22,0.48 ± 0.11 and 0.60 ± 0.23,respectively,and the difference was statistically significant (P ＜ 0.05).Western blotting results were consistent with Real-time PCR results.Flow cytometry results showed that compared with the control group,the proportion of cells located in G0/G1 phase in the experimental group increased (P ＜ 0.05),suggesting that the cells were arrested in G0/G1 phase.MTT assay showed that the viability of 769-P and ACHN cells in the experimental group was significantly lower than that in the control group.Colony formation experiments showed that the number of colony formation in the experimental group was significantly less,suggesting that the cell proliferation capacity decreased.Conclusion miR-103b can inhibit the growth of renal cell carcinoma cells by activating the expression of P21 protein and blocking the progression of the renal cell cycle,which provides a theoretical basis for the molecular targeted therapy of renal cell carcinoma.
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<p><b>OBJECTIVE</b>To explore the feasibility and safety of Bishop-Koop stoma procedure in the treatment of neonates with refractory congenital intestinal atresia.</p><p><b>METHODS</b>Clinical and follow-up data of 25 neonates with refractory congenital intestinal atresia undergoing Bishop-Koop stoma procedure in our center from January 2011 to December 2014 were retrospectively analyzed. Of 25 neonates, 13 (52%) were male, 12(48%) were female, the birth weight was 1600-3800 g (mean 2920 g), the age of admission was 10 hours to 20 days, and the age of operation was 1-58 d (mean 7 d). Diameter ratio of proximal atresia intestine to distal atresia intestine was all greater than 4. Eleven cases(44%) were high jejunal atresia, 3 cases(12%) type III( b, 7 cases(28%) type IIII(, 14 cases(56%) were identified as complex meconium peritonitis, and 3 cases (12%) received reoperation.</p><p><b>RESULTS</b>All the cases completed their Bishop-Koop stoma operations successfully with median operative time of 3 (1.2-4.5) hours and median intra-operative blood loss of 3.5(1-18) ml. The postoperative complication rate was 20%(5/25), including 3 cases of cholestasis, 1 case of ileus, and 1 case of neonatal necrotizing enterocolitis with septicemia who died 6 days after operation resulting in the mortality of 4%. Besides, 1 case gave up treatment because of economic reason. For the rest 23 neonates, the median first feeding time was 11 days and mean time was 11(5 to 20) days; the median time of postoperative total parenteral nutrition (TPN) was 15 days and mean time was 21 (5 to 68) days; the median hospital stay was 33 days and mean hospital stay was 25(12 to 81) days, respectively. Two-stage stoma closure operations were performed in all the 23 cases afterwards and no postoperative associated complications were found. When discharge after Bishop-Koop stoma operations, Z score of body weight was normal in 3 cases(13.0%) and lower than normal in 20 cases(87.0%), while in hospitalization for stoma closure, Z score of body weight was normal in 19 cases(82.6%) and lower than normal in 4 cases (17.4%). Of 23 cases, serum albumin level was normal in 9 cases(39.1%) before operation, in 3 cases (13.0%) when discharge and in 22 cases(95.7%) in hospitalization for stoma closure.</p><p><b>CONCLUSION</b>Bishop-Koop stoma procedure is safe and feasible in the treatment of neonates with refractory congenital intestinal atresia, and can obviously improve the nutritional status.</p>