Background MicroRNA-200c (miR-200c) is one of the short noncoding RNAs that play crucial roles in tumorigenesis and tumor progression. It also acts as considerable modulator in the process of epithelial-to-mesenchymal transition (EMT), a cell development regulating process that affects tumor development and metastasis. However, the role of miR-200c in bladder cancer cells and its mechanism has not been well studied. The purpose of this study was to determine the potential role of miR-200c in regulating EMT and how it contributed to bladder cancer cells in invasion, migration and proliferation. Methods Real-time reverse transcription-PCR was used to identify and validate the differential expression of MiR-200c involved in EMT in 4 bladder cancer cell lines and clinical specimens. A list of potential miR-200 direct targets was identified through the TargetScan database. The precursor of miR-200c was over-expressed in UMUC-3 and T24 cells using a lentivirus construct, respectively. Protein expression and signaling pathway modulation were validated through Western blot analysis and confocal microscopy, whereas BMI-1 and E2F3, direct target of miR-200c, were validated by using the wild-type and mutant 3’-untranslated region BMI-1/E2F3 luciferase reporters. Results We demonstrate that MiR-200c is down-regulated in bladder cancer specimens compared with adjacent ones in the same patient. Luciferase assays showed that the direct down-regulation of BMI-1 and E2F3 were miR-200c-dependent because mutations in the two putative miR-200c-binding sites have rescued the inhibitory effect. Over-expression of miR-200c in bladder cancer cells resulted in significantly decreased the capacities of cell invasion, migration and proliferation. miR-200c over-expression resulted in conspicuous down-regulation of BMI-1and E2F3 expression and in a concomitant increase in E-cadherin levels. Conclusions miR-200c appears to control the EMT process through BMI-1 in bladder cancer cells, and it inhibits their proliferation through down-regulating E2F3. The targets of miR-200c include BMI-1 and E2F3, which are a novel regulator of EMT and a regulator of proliferation, respectively.

BACKGROUND:In view of the fact that JS-K might regulate ubiquitin E3 ligase and that ubiquitin E3 ligase plays an important role in the mechanism of CRPC formation, the goal was to investigate the probable mechanism by which JS-K regulates prostate cancer cells.METHODS:Proliferation inhibition by JS-K on prostate cancer cells was examined usingCCK-8 assays. Caspase 3/7 activity assays and flow cytometry were performed to examine whether JS-K induced apoptosis in prostate cancer cells. Western blotting and co-immunoprecipitation analyses investigated JS-K's effects on the associated apoptosis mechanism. Real time-PCR and Western blotting were performed to assess JS-K's effect on transcription of specific AR target genes. Western blotting was also performed to detect Siah2 and AR protein concentrations and co-immunoprecipitation to detect interactions of Siah2 and AR, NCoR1 and AR, and p300 and AR.RESULTS:JS-K inhibited proliferation and induced apoptosis in prostate cancer cells. JS-K increased p53 and Mdm2 concentrations and regulated the caspase cascade reaction-associated protein concentrations. JS-K inhibited transcription of AR target genes and down-regulated PSA protein concentrations. JS-K inhibited Siah2 interactions and also inhibited the ubiquitination of AR. With further investigation, JS-K was found to stabilize AR and NCoR1 interactions and diminish AR and p300 interactions.CONCLUSIONS:The present results suggested that JS-K might have been able to inhibit proliferation and induce apoptosis via regulation of the ubiquitin-proteasome degradation pathway, which represented a promising platform for the development of new compounds for PCa treatments.

The aim of the present study was to evaluate the functions of miR-200c in the regulation of tumor growth and metastasis in renal cancer cells, and to investigate the underlying mechanisms. In this study, miR-200c was up- and downregulated in two renal cancer cell lines, namely ACHN and A498, and the proliferation, colony formation, migration and invasion of the cells were measured. The expression levels of various mRNAs and proteins were then analyzed using reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. It was found that miR-200c suppressed proliferation, migration and invasion of the renal cancer cells and, conversely, the inhibition of endogenous miR-200c resulted in increased cell proliferation and metastasis. Furthermore, a luciferase reporter assay revealed that miR-200c directly targeted the 3' untranslated regions of the oncogenes B-cell-specific Moloney murine leukemia virus insertion site 1 (Bmi-1) and E2F transcription factor 3 (E2F3) mRNAs, reduced the expression of Bmi-1 and E2F3 and regulated the expression of downstream genes, including E-cadherin, N-cadherin, vimentin, p14 and p16. These results indicate a tumor suppressor role for miR-200c in renal cancer cells via the direct targeting of Bmi-1 and E2F3.

The aim of the present study was to investigate the effect of resveratrol on renal carcinoma cells and explore possible renin-angiotensin system-associated mechanisms. Subsequent to resveratrol treatment, the cell viability, apoptosis rate, cytotoxicity levels, caspase 3/7 activity and the levels of angiotensin II (AngII), AngII type 1 receptor (AT1R), vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2) were evaluated in renal carcinoma cells. The effects of AngII, AT1R, VEGF and COX-2 on resveratrol-induced cell growth inhibition and apoptosis were also examined. The results indicated that resveratrol treatment may suppress growth, induce apoptosis, and decrease AngII, AT1R, VEGF and COX-2 levels in renal carcinoma ACHN and A498 cells. In addition, resveratrol-induced cell growth suppression and apoptosis were reversed when co-culturing with AT1R or VEGF. Thus, resveratrol may suppress renal carcinoma cell proliferation and induce apoptosis via an AT1R/VEGF pathway.

Reactive oxygen species (ROS) are chemical species that alter redox status, and are responsible for inducing carcinogenesis. The purpose of the present study was to assess the effects of the glutathioneS transferaseacti-vated nitric oxide donor prodrug, JS-K, on ROS accumulation and on proliferation and apoptosis in human prostate cancer cells. Cell proliferation and apoptosis, ROS accumulation and the activation of the mitochondrial signaling pathway were measured. The results demonstrated that JS-K may inhibit prostate cancer cell growth in a dose- and time-dependent manner, and induce ROS accumulation and apoptosis in a dose-dependent manner. With increasing concentrations of JS-K, expression of pro-apoptotic proteins increased, but Bcl-2 expression decreased. Additionally, the antioxidant N-acetylcysteine reversed JS-K-induced cell apoptosis; conversely, the pro-oxidant glutathione disulfide exacerbated JS-K-induced apoptosis. In conclusion, the data suggest that JS-K induces prostate cancer cell apoptosis by increasing ROS levels.

Objective: To investigate medical postgraduates'quality of life ( QOL) and its influencing factors, to provide support for interven-tions.Methods:495 medical postgraduates were surveyed with the World Health Organization Quality of Life-Brie (QOL-B).Results: The scores of physiology, psychology, social relationship and environment domain were (61.40 ±11.91), (58.61 ±12.79), (60.71 ±15.62) and (52.91 ±13.82) respectively.In psychological field of quality of life, the scores of medical postgraduates from the most harmonious family are higher than the others; in physical and psychological field, the scores of the first-grader medical postgraduates were higher than the second-grade, and the scores of the Second-grade medical postgraduates are higher than the Third-grade.In social relationship and environmental field of quality of life, the scores of married postgraduates were higher than the unmarried.In physical, psychological and environmental field, the scores of medical postgraduates from the university of 985, 211 were higher than the others; The higher degree of professional satisfaction, the higher the quality of life score in all field; Logistic regression analysis showed the degree of professional satisfaction and health status influence medical postgraduates'self-evaluation of quality of life.Conclusion: Overall, the QOL of medical postgraduates is good, the degree of profes-sional satisfaction, health status, marriage and grades are the influencing factors of the QOL of medical postgraduates.

前列腺癌是男性最常见的肿瘤之一.一氧化氮(nitric oxide,NO)作为生物信使或效应分子在体内发挥重要的生理作用,且其体内水平异常与多种疾病的发生和发展密切相关.因此,一氧化氮前体型药物的研究备受关注.一些NO前体药物已被证实具有良好的抗肿瘤活性,显示出广泛的临床应用潜力和价值.目前,NO前体药物中显示出显著抗肿瘤效应的主要有有机硝酸酯、硝普盐、S-亚硝基硫醇和偶氮二醇烯鎓盐等.一氧化氮前体药可通过靶向释放NO,直接杀伤肿瘤细胞、诱导肿瘤细胞凋亡、增强免疫系统作用、削弱肿瘤细胞增殖及侵袭能力,并抑制其转移,提高肿瘤细胞对放化疗的敏感度,从而发挥抗肿瘤作用.本文就近年来NO前体药物对前列腺癌作用的研究进展作一综述.

目的 探讨影响前列腺癌患者生存质量的相关因素.方法 采用世界卫生组织生存质量简表(WHOQOL-BREF)、家庭功能评估量表(APGAP)和抑郁自评量表(SDS)对我院泌尿外科住院的113名前列腺癌患者进行问卷调查.结果 全部113名前列腺癌患者生存质量得分生理、心理、社会关系和环境领域得分分别为(48.57±13.25)、(41.42±11.93)、(52.34±12.65)和(60.63±13.94)分;生理、心理、社会关系、环境领域生存质量得分高收入患者高于低收入患者(F=3.55、4.17、3.99、3.72,P＜0.05),医保、新农合患者高于自费患者(F=5.44、3.94、6.04、6.22,P＜0.05),无尿道压迫症状患者高于有尿道压迫症状患者(t =-2.22、-2.98、-2.03、-2.44,P＜0.05);生理、心理和环境领域生存质量得分高文化程度患者高于低文化程度患者(F=3.16、3.67、8.68,P＜0.05);生理、心理和社会关系领域生存质量得分病程短的患者高于病程长的患者(F=3.92、4.30、3.53,P＜0.05),单纯手术患者高于其他治疗方式的患者(F=10.42、7.37、4.42,P＜0.05);家庭功能障碍越严重,生存质量得分越低(F=6.66、4.02、3.79、1.68,P＜0.05),抑郁状况越严重,生存质量得分越低(F=4.36、6.43、3.45、4.81,P＜0.05);Logistic回归分析显示经济状况、尿道压迫症状、家庭功能和抑郁状况是前列腺癌患者生存质量自我综合评分的影响因素.结论 前列腺患者生存质量的影响因素主要有经济状况、付费方式、文化程度等.家庭功能、抑郁状况与前列腺癌患者生存质量明显相关.应充分利用家庭和社会的力量重视患者的身心健康,以提高前列腺患者的生存质量.

microRNA(miRNA)是内源性非编码单链小RNA,参与细胞增殖、凋亡与分化等多种重要生命活动的调控.近年来研究发现,miRNAs参与多种恶性肿瘤的演进,起抑癌基因或原癌基因的作用.miR-200c是上皮-间质转化(epithelial-mesen-chymal,EMT)过程中的重要调节基因,除了在正常细胞的表型转换中起作用,还在多种类型癌细胞的表型转换中起调节作用,能促进或者抑制肿瘤的侵袭转移能力.此外,关于miR-200c的研究还涉及肿瘤的耐药性和凋亡抗性.研究证实,miR-200c能够促进或抑制肿瘤的侵袭转移,逆转肿瘤细胞的耐药性和凋亡抗性.本文主要对不同肿瘤中miR-200c对肿瘤进展的影响进行综述.

Melioidosis is a fatal, endemic disease caused by Burkholderiapseudomallei which is a gram-negative bacillus. Melioidosis present diversely that ranging from chronic disease to fulminant sepsis, and may affect almost any organ in the body. And in China, melioidosis presenting primarily as prostatic abscesses has rarely been reported. Rapid and accurate diagnostics are needed for melioidosis as the clinical presentation is nonspecific and treatment requires specific antibiotics. Here, we report the clinic features of two cases of prostatic melioidosis that we had cured during 1995 to 2015 and discuss its diagnosis and specific treatment.

MicroRNA作为生物小分子参与调控机体内环境稳态和许多疾病发生与发展的过程。Let-7是目前研究最为广泛microRNA之一,在多种肿瘤中表达下调,提示let-7与肿瘤存在一些重要的联系。本文主要讨论let-7家族与肿瘤的研究进展,以进一步了解肿瘤发病机制,为肿瘤的预防和诊治提供新思路。

Reactive oxygen species (ROS) and cellular oxidant stress are regulators of cancer cells. The alteration of redox status, which is induced by increased generation of ROS, results in increased vulnerability to oxidative stress. The aim of this study is to investigate the influence of O-2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl) piperazin-1-yl]diazen-1-ium-1,2-diolate (JS-K, C13H16N6O8) on proliferation and apoptosis in bladder cancer cells and explored possible ROS-related mechanisms. Our results indicated that JS-K could suppress bladder cancer cell proliferation in a concentration- and time-dependent manner and induce apoptosis and ROS accumulation in a concentration-dependent manner. With increasing concentrations of JS-K, expression of proteins that are involved in cell apoptosis increased in a concentration-dependent manner. Additionally, the antioxidant N-acetylcysteine (NAC) reversed JS-K-induced cell apoptosis; conversely, the prooxidant oxidized glutathione (GSSG) exacerbated JS-K-induced cell apoptosis. Furthermore, we found that nitrites, which were generated from the oxidation of JS-K-released NO, induced apoptosis in bladder cancer cells to a lower extent through the ROS-related pathway. In addition, JS-K was shown to enhance the chemo-sensitivity of doxorubicin in bladder cancer cells. Taken together, the data suggest that JS-K-released NO induces bladder cancer cell apoptosis by increasing ROS levels, and nitrites resulting from oxidation of NO have a continuous apoptosis-inducing effect.

Epithelioid angiomyolipoma (EAML) is a rare renal mesenchymal tumor with malignant potential and is frequently associated with tuberous sclerosis complex (TSC). As metastasis of the tumor cells occur early, EAML is considered a potentially malignant tumor type and intrigues further research on it. Under the microscope, we could find the tumor was composed of atypical polygonal cells sheet mixed with classic angiomyolipoma (AML) components such as blood vessels with notable thick vascular walls, smooth muscle-like cells and adipocytes. Immunohistochemical studies showed that epithelioid cells were focally positive for vimentin, melanocytic markers (HMB-45), myoid markers (α-smooth muscle actin), CD34 and CD68; negative for cytokeratin, epithelial membrane antigen, CD10, and S-100. And the Ki67 index showed approximately 3%. Here, we report the morphological and immunohistochemical features of clinically or histologically malignant renal EAML and discuss its diagnosis, differential diagnosis and the prognosis.

BACKGROUND:MicroRNA-429 (miR-429), a short noncoding RNA belonging to the miR-200 superfamily, plays a crucial role in tumorigenesis and tumor progression. It also acts as a modulator of epithelial-to-mesenchymal transition, a cell development regulating process that affects tumor development and metastasis. The aim of this study was to investigate the potential role of miR-429 in regulating growth and metastasis of renal cell carcinoma.METHODS:miR-429 expression was stably up-regulated or down-regulated in the renal cell carcinoma ACHN and A498 cell lines, and cell proliferation and metastasis were assessed.RESULTS:miR-429 overexpression inhibited cell proliferation, colony formation, migration, and invasion. Suppression of endogenous miR-429 promoted cell growth and metastasis. miR-429 was shown to directly target the 3' untranslated regions of B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) and E2F transcription factor 3 (E2F3) transcripts, regulating their expression, as well as that of the downstream epithelial-to-mesenchymal transition markers E-cadherin, N-cadherin, vimentin, p14, and p16.CONCLUSIONS:These results revealed a tumor suppressive role for miR-429 in renal cell carcinoma through directly targeting BMI1 and E2F3.

Under different circumstances,nitric oxide (NO) can act as cellular signaling molecule,toxicant and antioxidant in physiological and pathological process.O2-(2,4-dinitrophenoxy)-1-[(4-ethoxycarbonyl) piperazin-1-yl] diazen-1-ium-1,2-diolate (JS-K),a prodrug of NO,is a type of diazeniumdiolates,which can be activated by glutathione-S-transfarase (GST) and release NO at a high concentration.This activation can accelerate the apoptosis of tumor cells by promoting mitogen-activated protein kinase (MAPK) pathway and caspase cascade reaction,suppressing ubiquitin system and β-catenin/ T cell factor (TCF) pathway,and inducing DNA damage.With the advances in this field,the more creative methods emerged to apply JS-K in anti-tumor therapy and can make the treatment more effective,safe and accurate.This paper reviews the relationship between JS-K and apoptosis of tumor cells.

目的:将皮内着色技术应用到脱毛后的昆白小鼠,研究脱发的美容方法,从全新的角度对男性脱发进行美容.方法:将昆白鼠去除背部毛发后,用文身机刺针进行皮内着色,并将着色染料进行分级.结果:皮内着色后的小鼠无不良反应,着色效果佳,持久时间长,未见明显褪色,部分针刺点有局部晕色现象,可以通过调节进针深度而改善.结论:皮内着色无论是持续时间还是美观效果角度,比现有手段都更有优势,值得进一步研究,以得到更安全的着色剂,并进行临床试验.

The aim of this study was to investigate the function of miR-183 in renal cancer cells and the mechanisms miR-183 regulates this process. In this study, level of miR-183 in clinical renal cancer specimens was detected by quantitative real-time PCR. miR-183 was up- and down-regulated in two renal cancer cell lines ACHN and A498, respectively, and cell proliferation, Caspase 3/7 activity, colony formation, in vitro migration and invasion were measured; and then the mechanisms of miR-183 regulating was analyzed. We found that miR-183 was up-regulated in renal cancer tissues; inhibition of endogenous miR-183 suppressed in vitro cell proliferation, colony formation, migration, and invasion and stimulated Caspase 3/7 activity; up-regulated miR-183 increased cell growth and metastasis and suppressed Caspase 3/7 activity. We also found that miR-183 directly targeted tumor suppressor, specifically the 3'UTR of three subunits of protein phosphatase 2A (PP2A-C alpha, PP2A-C beta, and PP2A-B56-gamma) transcripts, inhibiting their expression and regulated the downstream regulators p21, p27, MMP2/3/7 and TIMP1/2/3/4. These results revealed the oncogenes role of miR-183 in renal cancer cells via direct targeting protein phosphatase 2A. (C) 2014 Elsevier Inc. All rights reserved.