血管内皮生长因子、血小板反应素1在肾上腺皮质肿瘤中的表达及其意义

目的讨论血管内皮生长因子（VEGF）与血小板反应素1（TSP-1）在肾上腺皮质肿瘤中的表达及其临床意义。方法选取经手术治疗且取得完整临床资料的肾上腺皮质肿瘤石蜡包埋标本37例,其中良性组20例,恶性组（ACC组）17例。采用免疫组化技术,检测并分析良、恶性肾上腺皮质肿瘤中VEGF和TSP-1的表达情况。结果TSP-1在ACC组中呈低表达（5／17,29．41％）,在良性组中表达高（13／20,65．00％）,ACC组与良性组之间TSP-1的表达有显著性差异（P〈0．05）。VEGF在ACC组中呈高表达（70．59％）,在良性组中表达较低（25．00％）,VEGF在ACC组中的表达与在良性组中的表达有显著性差异（P〈0．05）。微血管密度（MVD）在ACC组中的表达为（76．40±15．64）／视野,良性组中为（21．05±8．07）／视野,两者之间有显著性差异（P〈0．05）。VEGF的表达和MVD呈正相关（P〈0．01）,TSP-1的表达和MVD呈负相关（P〈0．01）。VEGF的表达和TSP-1的表达呈负相关（rs＇=-0．386）。结论VEGF与TSP-1表达不平衡可能是肾上腺皮质肿瘤肿瘤性血管生成的重要原因,有望为抗肿瘤靶向治疗在ACC中的应用提供相应的理论依据。     

MicroRNA‐494 Promotes Cyclosporine‐Induced Nephrotoxicity and Epithelial to Mesenchymal Transition by Inhibiting PTEN

A major complication associated with cyclosporine (CsA) treatment is nephrotoxicity. In this study, we examined whether microRNAs play a role in cyclosporine‐induced nephrotoxicity. Treatment of mice with CsA resulted in nephrotoxicity that was associated with an early increase in expression of microRNA mmu‐miR‐494 (miR‐494). Similarly, tubular epithelial cell epithelial‐mesenchymal transition (EMT) induced by CsA toxicity resulted in the upregulation of microRNA‐494 and a decrease in PTEN levels in vitro. miR‐494 directly targeted Pten and negatively regulated its expression. Preventing Pten targeting by miR‐494 was sufficient to prevent CsA induced EMT. Knockdown of miR‐494 prevented the downregulation of PTEN in tubular epithelial cells following CsA treatment and also prevented CsA induced EMT. Thus, miR‐494 plays a major role in promoting CsA induced nephrotoxicity through its ability to target Pten thereby contributing to EMT. We suggest that manipulating miR‐494 expression may represent a novel approach to preventing EMT associated with CsA induced nephrotoxicity.     

黄连素调节miR-29b抑制高糖诱导的MPC-5足细胞上皮-间质转化研究

[目的]探讨miR-29b在高糖诱导的MPC-5足细胞上皮-间质转化中的作用及黄连素的保护机制.[方法]将MPC-5小鼠足细胞分为正常组、高糖组和高糖+50μmol/L黄连素组,培养48 h后,采用酶联免疫吸附法(ELISA)测定培养液上清液中的重组人转化生长因子-β1(TGF-β1),实时定量聚合酶链反应(RT-qP...     

CIAPIN1 as a therapeutic target in cancer

Importance of the field: Cytokine-induced apoptosis inhibitor 1 (CIAPIN1) is a newly identified cytokine-induced apoptosis inhibitor, which has roles in cell division and angiogenesis. Owing to its prognostic value for human tumors and involvement in cancer progression and tumor cell resistance to anticancer agents, CIAPIN1 has been proposed as an attractive target for new anticancer interventions.

Areas covered in this review: We define CIAPIN1's potential function as a new therapeutic target for anticancer interventions and this review covers all related literature on CIAPIN1 in cancer from the past 5 years

What the reader will gain: Several preclinical studies have demonstrated that CIAPIN1 is associated with chemotherapy resistance, increased tumor recurrence and shorter patient survival in different human tumor models, making anti-CIAPIN1 therapy an attractive cancer treatment strategy. Recent studies also suggest that CIAPIN1 is expressed at low levels in some types of malignant tumors and that its overexpression may inhibit their proliferation or tumorigenesis.

Take home message: Considering that the exact expression and function of CIAPIN1 are still not well characterized and understood, better knowledge of CIAPIN1 in normal versus tumor tissues will be instrumental for the design of optimal strategies to selectively disrupt CIAPIN1 in cancer.