Retracted: Upregulation of long noncoding RNA TUG1 contributes to the development of laryngocarcinoma by targeting miR-145-5p/ROCK1 axis

Laryngocarcinoma is the most common head and neck cancer and has a high incidence and mortality, causing about 83 000 deaths per year worldwide. Our research aimed to investigate the possible role of long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in laryngocarcinoma development. The messenger RNA (mRNA) levels of TUG1 in tumor tissues and control (plasma) samples of laryngocarcinoma patients as well as in laryngocarcinoma cells were detected. The influences of TUG1 suppression on cell biological processes (viability, apoptosis, migration, and invasion) and cytoskeleton rearrangement in laryngocarcinoma cells were tested. Moreover, we investigated the regulatory interaction between TUG1 and miR-145-5p, and identified the target gene of miR-145-5p. The association between TUG1 and the protein expressions of RhoA/rho associated coiled-coil containing protein kinase (ROCK)/matrix metalloproteinases (MMPs) pathway-associated factors were detected. TUG1 was found to be highly expressed in tumor tissues and plasma samples of laryngocarcinoma patients as well as in laryngocarcinoma cells. Suppression of TUG1 decreased laryngocarcinoma cell viability, increased apoptosis, and suppression migration, invasion, and cytoskeleton rearrangement. Moreover, TUG1 negatively regulated miR-145-5p. TUG1 regulated tumor growth (viability and apoptosis) and metastasis through miR-145-5p. Furthermore, ROCK1 was targeted by miR-145-5p, and miR-145-5p/ROCK1 partner was involved in the process of tumor growth and metastasis. Finally, we found that TUG1 functioned on laryngocarcinoma by activating RhoA/ROCK/MMPs pathway. Our study reveals that lncRNA TUG1 is upregulated in laryngocarcinoma and may be involved in the process of laryngocarcinoma through miR-145-5p downregulation and activating the RhoA/ROCK/MMPs signals.     

鸡miR-21的组织表达谱及其功能预测分析

已知miR-21在多种生物学过程中发挥重要的调控作用,然而有关鸡miR-21功能的研究尚未见报道。为了解鸡miR 21的潜在生物学功能,采用qRT-PCR检测了固始鸡5个发育阶段、15种组织中miR-21的表达情况。同时,利用Pictar和TargetScan算法预测了miR-21的靶基因并对预测的靶基因进行了Gene Ontology分析和通路分析。结果显示,miR-21的表达具有明显的时序特征,除14胚龄鸡的小脑和腺胃外,胚胎期各组织中miR-21的表达水平均显著低于出壳后对应组织的表达水平;出壳后鸡的下丘脑、大脑、小脑、小肠、肝脏、胸肌和肾脏等组织中miR-21的表达水平随发育进程均显著上调。生物信息学分析显示,预测的miR-21的靶基因在基因表达调控、大分子代谢调控、转录调控、细胞代谢调控、细胞衰老和增殖、呼吸系统发育、骨骼发育、心脏发育和神经系统发育等广泛的生物学过程中显著富集。总之,鸡miR-21为广泛性时序表达miRNA,可能参与鸡出壳后诸多器官发育相关的生物学过程的调控。     

MicroRNA-221 promotes colorectal cancer cell invasion and metastasis by targeting RECK

MicroRNAs (miRNAs) have recently emerged as regulators of metastasis. We provide insight into the behavior of miR-221 in colorectal cancer (CRC) metastasis by showing that miR-221 is significantly upregulated in metastatic CRC cell lines and tissues. miR-221 overexpression enhances, whereas miR-221 depletion reduces CRC cell migration and invasion in vitro and metastasis in vivo. We identify RECK as a direct target of miR-221, reveal its expression to be inversely correlated with miR-221 in CRC samples and show that its re-introduction reverses miR-221-induced CRC invasiveness. Collectively, miR-221 is an oncogenic miRNA which may regulate CRC migration and invasion through targeting RECK.     

MiR-144通过靶向抑制GRK5表达促进脊髓星形胶质细胞活化

已知miR-144与细胞活化和增殖有关,然而其具体分子机制尚不明确。本研究发现miR-144通过靶向GRK5促进脊髓星形胶质细胞的活化。运用real-time PCR检测脊髓损伤和正常大鼠的脊髓组织及其脊髓星形胶质细胞中miR-144的表达,发现与正常的组织和细胞相比,miR-144在脊髓损伤组织和星形胶质细胞中的表达水平显著降低;Western印迹检测到脊髓损伤大鼠的星形胶质细胞中GFAP蛋白的表达显著低于正常大鼠,而GRK5蛋白的表达高于正常大鼠;MTT分析结果显示转染miR-144可显著提高脊髓损伤大鼠的星形胶质细胞活性,但对细胞增殖无明显作用;酶活性试剂盒分析发现miR-144显著提高了SOD和GSH活性;生物学信息分析和萤光素酶报告基因检测结果显示miR-144能靶向结合GRK5,并下调GRK5的表达;MiR-144 mimic转染或miR-144 mimic与pcDNA-GRK5共转染脊髓损伤的星形胶质细胞,发现miR-144转染能通过激活NF-κB通路消除pcDNA-GRK5引起的细胞活化抑制。综上所述,miR-144通过靶定结合癌基因GRK5来促进脊髓星形胶质细胞细胞的活化。     

MiR-27靶基因的分析及鉴定

MicroRNAs(miRNAs)是一类约20～25nt的小分子核苷酸,在细胞内的多种生物学过程,如细胞增殖、凋亡、生长、分化和代谢等过程中具有重要的功能。已知miR-27在脂肪细胞和肌肉细胞的发育过程中起了重要作用,其在神经细胞中的表达调节至今仍不清楚。在本研究中,通过miRBase和TargetScan数据库分析了miR-27的靶基因,构建了miR-27的真核表达载体,改造了萤火虫荧光素酶和海肾荧光素酶报告载体,将miR-27的靶基因Bmi1的3′-UTR融合到报告载体中,转染神经胶质瘤细胞,利用双荧光素酶检测系统分析荧光素酶的活性。研究发现miR-27a和miR-27b共同的靶基因主要调节发育过程。MiR-27真核表达载体能产生成熟态的miR-27。MiR-27a、miR-27b或miR-27a和miR-27b联合与Bmi1的3′-UTR的正义序列共转染U343细胞能明显降低萤火虫荧光素酶的活性(分别P0.05,P0.05,P0.01),这提示了Bmi1可能为miR-27的靶基因。