MicroRNA-21 via Dysregulation of WW Domain-Containing Protein 1 Regulate Atrial Fibrosis in Atrial Fibrillation

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MicroRNA-494-dependent WDHDI inhibition suppresses epithelial-mesenchymal transition,tumor growth and metastasis in cholangiocarcinoma

Background

Cholangiocarcinoma (CCA) represents a devastating malignancy characterized by high mortality, and notoriously problematic to diagnose. Recently, microRNAs (miRs) have been intensively investigated due to their potential usefulness from a tumor treatment perspective.

miR-98对肝癌 HepG2细胞增殖、凋亡以及侵袭、迁移能力的影响

目的：研究 miR-98对肝癌 HepG2细胞增殖、凋亡和侵袭、迁移能力的影响及其可能机制。方法将 miR-98mimics、mimics-NC、miR-98inhibitor、inhibitor-NC 瞬时转入肝癌 HepG2细胞内,应用噻唑盐( MTT)法、流式细胞仪、Tr-answell 小室实验检测 miR-98对肝癌 HepG2细胞增殖、凋亡以及侵袭、迁移能力的影响,进一步用 Western blot 法检测各组 Bcl-2蛋白的表达水平。结果 MTT 实验表明 miR-98过表达后,肝癌细胞的增殖能力明显低于对照组;Annexin V-FITC / PI 凋亡实验证实上调 miR-98表达后,细胞的凋亡率较对照组升高;Transwell 小室实验表明上调 miR-98可使肝癌细胞的侵袭、迁移能力减弱。而当 miR-98被抑制后,肝癌HepG2细胞的增殖及侵袭、迁移能力则明显增强,凋亡率则下降。 Western blot 实验检测发现 miR-98过表达后,Bcl-2的表达降低。结论 miR-98可能在肝癌的发生、发展中发挥着抑癌基因的作用;miR-98可能通过下调 Bcl-2的表达,促进肝癌 HepG2细胞凋亡。     

骨肉瘤患者血浆中microRNA-181b水平的检测

目的检测骨肉瘤患者血浆中microRNA-181b (miR-181b)的水平变化,初步探讨其临床意义.方法选择25例骨肉瘤患者和30例健康对照,采用茎-环定量逆转录聚合酶链反应(RT-PCR)方法检测血浆中miR-181b的水平,并分析miR-181b与骨肉瘤临床病理指标之间的关系.结果骨肉瘤患者血浆中miR-181b水平(0.62±0.25)与正常对照组(0.41±0.18)相比明显升高,差异具有统计学意义(P＜0.01);骨肉瘤患者血浆中miR-181b的水平与患者性别、年龄、肿瘤大小、肿瘤部位、病理类型及Enneking分期均无明显相关性(P＞0.05).结论骨肉瘤患者血浆中miR-181b水平增高,miR-181b可能参与了骨肉瘤的发病过程.     

MicroRNA-200a inhibits epithelial-mesenchymal transition in human hepatocellular carcinoma cell line

Objective: Our study investigated the role of microRNA (miR)-200a and its molecular targets in hepatocellular carcinoma (HCC) cells. Methods: An inhibitor of miR-200a was transiently transfected into the hepatocellular carcinoma cell line, MHCC-97L. The effect of this transfection on mRNA levels of epithelial-mesenchymal transition (EMT)-related genes was measured by fluorescence-based quantitative real-time polymerase chain reaction (qRT-PCR). Further, protein levels of EMT-related genes, cell proliferation and apoptosis-related markers were assessed by Western blot analysis in these transfected cells. MTT and wound-healing assay were used to evaluate the proliferation and migration of MHCC-97L cells in presence and in absence of miR-200a inhibitor. Results: Compared with miR-NC control group, qRT-PCR results in anti-miR-200a group revealed a significant reduction in the mRNA levels of E-cadherin, with a concomitant increasing in vimentin mRNA level (all P < 0.05). Western blot results showed higher E-cadherin and Caspase-3 protein expressions in anti-miR-200a group compared to miR-NC group (P < 0.05). In addition, vimentin and Ki-67 protein expression was found sharply decreased in anti-miR-200a group compared to miR-NC group (P < 0.05). Consistent with this, wound-healing and MTT assay showed that migration and proliferation capacity of MHCC-97L cells in anti-miR-200a group is significantly increased compared with miR-NC group (both P < 0.05). Conclusion: Our study reveals an important role of miR-200a in inhibiting EMT, proliferation and migration in HCC cells, suggesting the possibility of miR-200a-based therapeutics in HCC.     

Diagnostic significance of miR-106a in gastric cancer

As one of the most common malignant tumors, gastric cancer still lacks tumor markers with enough specificity and sensitivity. Therefore the development of novel tumor markers is necessary for early diagnosis in clinics. MicroRNA (miR) has been known to be of unique expressional patterns in various tumors and may work as potential tumor markers for clinical use. This study thus explored the significance of plasma miR-106a in clinical diagnosis of gastric cancer and its effects on proliferation of cancer cells. Plasma miR-106a levels were quantified by real-time quantitative fluorescent PCR methods in 80 cases of gastric cancer patients and healthy individuals to analyze the correlation between miR-106a and clinical features. MiR-106 inhibitor was further transfected into human gastric carcinoma cells for further cell proliferation using CCK-8 approach. MiR-106a was significantly up-regulated in gastric cancer patient plasma samples compared to healthy individuals (P<0.01). The area under ROC curve was 0.895 (95% CI: 0.846~0.943). It has a specificity of 93.8% and a sensitivity of 77.5% in diagnosing gastric cancer. MiR-106a level was also correlated with cancer differentiation stage, lymph node metastasis, TNM stage and tumor size (P<0.05). The down-regulation of miR-106 in gastric carcinoma cells inhibited cell proliferation (P<0.05). MiR-106a was significantly up-regulated in gastric cancer patients and can facilitate the in vitro proliferation of tumor cells. It may work as a biological marker for gastric cancer.     

Role of CD98 in liver disease

CD98 is a multifunctional glycoprotein that is involved in various biological processes such as amino acid transport, cell adhesion, diffusion, adhesion, and proliferation. The role of CD98 in liver disease has not thoroughly been examined and is limited reports in the literature. Among these reports, direct association for CD98 in nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC) have been reported. Our lab has reported that targeting CD98 in high fat diet mice reduced steatosis and inflammation in NAFLD. Other reports associate CD98 in HCC due in part to the role of CD98 in activating integrin signaling. Herein, we present CD98 staining on liver biopsies from NAFLD, chronic active hepatitis, cirrhosis, and 3 stages of HCC to demonstrate the upregulation of CD98 expression throughout liver disease progression. In addition, we analyze current literature to elucidate roles and potential roles of CD98 with each stage of liver disease.     

子宫内膜癌组织微小RNA-373表达情况及其对子宫内膜癌细胞增殖、迁移的影响研究

背景微小RNA-373 (miRNA-373)在多种恶性肿瘤(如肝癌、肺癌)的发生发展过程中具有重要作用,但其在子宫内膜癌(EC)发生发展中的作用尚不完全清楚。目的探讨EC组织miRNA-373表达情况及其对EC细胞增殖、迁移的影响。方法选取2012年6月-2013年6月在邯郸市妇幼保健院行手术治疗的64例EC患者的EC组织作为试验组,另选取同期在邯郸市妇幼保健院行子宫切除术的30例良性子宫肌瘤患者的正常组织作为对照组。采用实时荧光定量聚合酶链反应(qRT-PCR)检测两组miRNA-373表达情况,绘制Kaplan-Meier生存曲线以分析不同miRNA-373表达情况EC患者术后5年预后;分别比较转染miRNA-373模拟物(miRNA-373 mimic)及其阴性对照物(mimic-NC)、miRNA-373抑制剂(miRNA-373 inhibitor)及其阴性对照物(inhibitor-NC)的HEC-1B细胞大型肿瘤抑制基因2 (LATS2)表达情况、转染96 h后吸光度值、迁移细胞数量;采用双荧光素酶报告基因系统验证miRNA-373与LATS2间的靶标关系。结果 (1)试验组miRNA-373相对表达量高于对照组(P<0.05)。根据miRNA-373相对表达量平均值将试验组患者分为低表达组(n=26)和高表达组(n=38),Kaplan-Meier生存曲线显示,高表达组患者术后5年累积生存率为52.6%,低于低表达组的84.6%(P<0.05)。(2)转染miRNA-373 mimic的HEC-1B细胞LATS2相对表达量低于转染mimic-NC的HEC-1B细胞(P<0.05);转染miRNA-373 inhibitor的HEC-1B细胞LATS2相对表达量高于转染inhibitor-NC的HEC-1B细胞(P<0.05)。转染96 h后,转染miRNA-373 mimic的HEC-1B细胞吸光度值高于转染mimic-NC的HEC-1B细胞(P<0.05);转染miRNA-373 inhibitor的HEC-1B细胞吸光度值低于转染inhibitor-NC的HEC-1B细胞(P<0.05)。转染miRNA-373 mimic的HEC-1B细胞中迁移细胞数量多于转染mimic-NC的HEC-1B细胞(P<0.05);转染miRNA-373 inhibitor的HEC-1B细胞中迁移细胞数量少于转染inhibitor-NC的HEC-1B细胞(P<0.05)。(3)双荧光素酶报告基因系统检测结果显示,LATS2含有miRNA-373的潜在结合位点。野生型LATS2中miRNA-373相对荧光强度低于空载对照(P<0.05);突变型LATS2中miRNA-373相对荧光强度与空载对照比较,差异无统计学意义(P>0.05)。结论 EC组织miRNA-373呈高表达,其可通过直接靶向调节LATS2的表达而促进EC细胞增殖、迁移,进而影响EC患者预后。     

MicroRNA-29与糖尿病及其并发症

小分子RNA(miR)是近年发现的一类广泛存在于动植物中的小分子非编码RNA,它通过抑制靶目标的转录或直接将其降解而发挥作用.miR-29是新近发现的与糖尿病及其并发症有密切关系的一类小分子RNA.研究发现,miR-29可直接参与糖尿病的基本病理生理过程,如参与胰岛素相关信号通路.同时也参与肾脏纤维化、视网膜神经元凋亡等过程,从而在糖尿病肾病、糖尿病视网膜病变等糖尿病并发症的发生中起重要作用.