m iR NAs 的研究进展

MicroRNAs（miRNAs）是一种大小约21—23个碱基的单链小分子RNA,广泛存在于真核生物中。miRNAs在物种间具有高度的保守性、时序性和组织特异性。miRNAs可以通过部分互补或者完全互补结合到目的靶mRNA,以诱发蛋白质翻译抑制（翻译抑制子）或者介导目的mRNA的降解调节基因表达,参与生命过程中一系列的重要进程,包括细胞分化、生物发育、疾病的发生、发展,此外miRNAs还与病毒的复制和癌症等有关。miRNA作用和功能的揭示必定给nfiRNA的应用带来广阔前景。     

miR-761 regulates the mitochondrial network by targeting mitochondrial fission factor

Mitochondria are dynamic organelles that constantly undergo fission and fusion. The balance between fission and fusion determines the fate of the cell. In this study, we show that mitochondrial fission factor (MFF) is upregulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Knockdown of MFF attenuated hydrogen peroxide- and I/R injury-induced cardiomyocyte apoptosis and myocardial infarction. We found that MFF is a direct target of miR-761, and miR-761 inhibits mitochondrial fission and cardiomyocyte apoptosis by repressing MFF. This study reveals a novel model of mitochondrial fission regulation, which is composed of miR-761 and MFF. Modulation of their levels may provide a new approach for tackling apoptosis and myocardial infarction.     

miRNAs表达异常与宫颈癌发生发展关系的研究进展

宫颈癌(cervical cancer,CC)是严重危害女性健康的疾病之一,具有高的发病率和死亡率。微小RNA(miRNAs)是一类小分子非编码RNA,通过转录后沉默来调控基因表达。表达异常的miRNAs主要通过调控细胞周期、细胞凋亡以及多种信号通路的方式参与宫颈癌的发生发展。该文就近年来miRNAs在宫颈癌发生发展、诊断、治疗和预后评估等方面的研究进展做一综述,以寻求对宫颈癌的防治提供新思路。     

Downregulation of CCR1 inhibits human hepatocellular carcinoma cell invasion

CC chemokine receptor 1 (CCR1) has an important role in the recruitment of leukocytes to the site of inflammation. The migration and metastasis of tumor cells shares many similarities with leukocyte trafficking, which is mainly regulated by chemokine receptor-ligand interactions. CCR1 is highly expressed in hepatocellular carcinoma (HCC) cells and tissues with unknown functions. In this study, we silenced CCR1 expression in the human HCC cell line HCCLM3 using artificial microRNA (miRNA)-mediated RNA interference (RNAi) and examined the invasiveness and proliferation of CCR1-silenced HCCLM3 cells and the matrix metalloproteinase (MMP) activity. The miRNA-mediated knockdown expression of CCR1 significantly inhibited the invasive ability of HCCLM3 cells, but had only a minor effect on the cellular proliferation rate. Moreover, CCR1 knockdown significantly reduced the secretion of MMP-2. Together, these findings indicate that CCR1 has an important role in HCCLM3 invasion and that CCR1 might be a new target of HCC treatment.     

Knockdown of astrocyte elevated gene-1 inhibits tumor growth and modifies microRNAs expression profiles in human colorectal cancer cells

Astrocyte elevated gene-1 (AEG-1), upregulated in various types of malignancies including colorectal cancer (CRC), has been reported to be associated with the carcinogenesis. MicroRNAs (miRNAs) are widely involved in the initiation and progression of cancer. However, the functional significance of AEG-1 and the relationship between AEG-1 and microRNAs in human CRC remains unclear. The aim of this study was to investigate whether AEG-1 could serve as a potential therapeutic target of human CRC and its possible mechanism. We adopted a strategy of ectopic overexpression or RNA interference to upregulate or downregulate expression of AEG-1 in CRC models. Their phenotypic changes were analyzed by Western blot, MTT and transwell matrix penetration assays. MicroRNAs expression profiles were performed using microarray analysis followed by validation using qRT-PCR. Knockdown of AEG-1 could significantly inhibit colon cancer cell proliferation, colony formation, invasion and promotes apoptosis. Conversely, upregulation of AEG-1 could significantly enhance cell proliferation, invasion and reduced apoptisis. AEG-1 directly contributes to resistance to chemotherapeutic drug. Targeted downregulation of AEG-1 might improve the expression of miR-181a-2^∗, -193b and -193a, and inversely inhibit miR-31 and -9^∗. Targeted inhibition of AEG-1 can lead to modification of key elemental characteristics, such as miRNAs, which may become a potential effective therapeutic strategy for CRC.