OBJECTIVE: To summarize the regulatory effect of non-coding RNA (ncRNA) on type H vessels angiogenesis of bone. METHODS: Recent domestic and foreign related literature about the regulation of ncRNA in type H vessels angiogenesis was widely reviewed and summarized. RESULTS: Type H vessels is a special subtype of bone vessels with the ability to couple bone formation. At present, the research on ncRNA regulating type H vessels angiogenesis in bone diseases mainly focuses on microRNA, long ncRNA, and small interfering RNA, which can affect the expressions of hypoxia inducible factor 1α, platelet derived growth factor BB, slit guidance ligand 3, and other factors through their own unique ways of action, thus regulating type H vessels angiogenesis and participating in the occurrence and development of bone diseases. CONCLUSION At present, the mechanism of ncRNA regulating bone type H vessels angiogenesis has been preliminarily explored. With the deepening of research, ncRNA is expected to be a new target for the diagnosis and treatment of vascular related bone diseases.
Humans ; RNA, Untranslated/genetics* ; RNA, Long Noncoding ; Bone Diseases/genetics* ; MicroRNAs/genetics* ; RNA, Small Interfering

Studies of human and mammalian have revealed that environmental exposure can affect paternal health conditions as well as those of the offspring. However, studies that explore the mechanisms that meditate this transmission are rare. Recently, small noncoding RNAs (sncRNAs) in sperm have seemed crucial to this transmission due to their alteration in sperm in response to environmental exposure, and the methodology of microinjection of isolated total RNA or sncRNAs or synthetically identified sncRNAs gradually lifted the veil of sncRNA regulation during intergenerational inheritance along the male line. Hence, by reviewing relevant literature, this study intends to answer the following research concepts: (1) paternal environmental factors that can be passed on to offspring and are attributed to spermatozoal sncRNAs, (2) potential role of paternal spermatozoal sncRNAs during the intergenerational inheritance process, and (3) the potential mechanism by which spermatozoal sncRNAs meditate intergenerational inheritance. In summary, increased attention highlights the hidden wonder of spermatozoal sncRNAs during intergenerational inheritance. Therefore, in the future, more studies should focus on the origin of RNA alteration, the target of RNA regulation, and how sncRNA regulation during embryonic development can be sustained even in adult offspring.
Animals ; Environmental Exposure ; Epigenesis, Genetic ; Female ; Humans ; Male ; Mammals/genetics* ; Pregnancy ; RNA, Small Untranslated/genetics* ; Spermatozoa

OBJECTIVETo evaluate interfering effect of several short interfering RNAs (siRNA) on HCV 5' untranslated region(5' UTR).

METHODSThe green fluorescent protein (GFP) was used as reporter gene. A fused gene of HCV-5'UTR and GFP was constructed. It was cloned into the plasmid pCDNA3.1 named as pcDNA-HCV-5'UTR-GFP. Three siRNAs were designed and transfected into HepG2 cells with pcDNA-HCV-5'UTR-GFP. The change of the fluorescence intensity of HepG2 cells was shown by fluorescence microscopy and numerically detected under 488 nm wave length by flow cytometry.

RESULTSThe fused gene of HCV-5'UTR and GFP was successfully constructed. The seven groups displayed inhibitory effects on the gene expression of GFP. The inhibition rates of siRNA A, B and C were 68.4 percent, 72.6 percent and 75.6 percent, respectively. The inhibitory rates of siRN A + B, siRN B +C and siRN A +C were 91.8 percent, 87.2 percent and 92.4 percent, respectively. The inhibitory rates of siRN A+B +C was the highest, up to 95.7 percent.

CONCLUSIONThese siRNAs could inhibit expression of HCV 5'UTR gene, the inhibitory effect of combined siRNA was better than that of single siRNAs.

5' Untranslated Regions ; genetics ; Green Fluorescent Proteins ; genetics ; Hepacivirus ; genetics ; RNA Interference ; RNA, Small Interfering ; genetics ; Transfection

Small RNAs (sRNA) are produced abundantly in either plants or animals and function in regulating gene expression or in defense against virus infection. Deep sequencing of small RNAs is an emerging technology in virus identification and de novo assembly of virus genomes and is demonstrated to be an effective method to discover new viruses and monitor virus variation. A significant number of viruses from plants, invertebrates and human cells has been successfully identified using this technology. In this paper, we summarized the principle, operation process and latest advances of sRNA deep sequencing We also showed the feasibility of sRNA deep sequencing by bioinformatic analysis using sRNA deep sequencing dataset public available for the detection of viruses.
Genomics ; High-Throughput Nucleotide Sequencing ; methods ; RNA, Small Untranslated ; genetics ; RNA, Viral ; genetics ; Sequence Analysis, RNA ; methods ; Viruses ; genetics ; isolation & purification

HIV-1 utilizes cellular factors for efficient replication. The viral RNA is different from cellular mRNAs in many aspects, and is prone to attacks by cellular RNA quality control systems. To establish effective infection, the virus has evolved multiple mechanisms to protect its RNA. Here, we show that expression of the Y-box binding protein 1 (YB-1) enhanced the production of HIV-1. Downregulation of endogenous YB-1 in producer cells decreased viral production. YB-1 increased viral protein expression by stabilizing HIV-1 RNAs. The stem loop 2 in the HIV-1 RNA packaging signal was mapped to be the YB-1-responsive element. Taken together, these results indicate that YB-1 stabilizes HIV-1 genomic RNA and thereby enhances HIV-1 gene expression and viral production.
5' Untranslated Regions ; Chromosome Mapping ; Down-Regulation ; HEK293 Cells ; HIV-1 ; genetics ; metabolism ; Humans ; Inverted Repeat Sequences ; Protein Binding ; RNA Interference ; RNA, Small Interfering ; metabolism ; RNA, Viral ; metabolism ; Virus Replication ; Y-Box-Binding Protein 1 ; antagonists & inhibitors ; genetics ; metabolism

Animals ; Apoptosis ; Cadherins ; genetics ; metabolism ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; metabolism ; physiology ; Neoplasm Invasiveness ; Neoplasms ; genetics ; metabolism ; pathology ; therapy ; RNA, Double-Stranded ; genetics ; metabolism ; physiology ; RNA, Small Interfering ; genetics ; metabolism ; physiology ; RNA, Small Untranslated ; genetics ; metabolism ; physiology ; therapeutic use ; Transcriptional Activation

OBJECTIVETo explore whether miR-200b suppresses tumor cell invasion by targeting PROM1, thus to reveal the molecular mechanism that miR-200b functions as a tumor suppressor in glioma.

METHODSPROM1 3'UTR-luciferase vector was constructed and dual-luciferase reporter gene assay was employed to examine the effect of miR-200b on luciferase activity. Human glioblastoma U87 cells were transfected with miR-200b mimics, and next qRT-PCR and Western blotting were performed to detect the expressions of PROM1 mRNA and protein. The effect of PROM1 down-regulation on invasion was observed after PROM1 siRNA were transfected into U87 cells.

RESULTSThe miR-200b bound to the 3'-untranslated region (UTR) of PROM1 and inhibited the luciferase activity. Its luciferase activity was down-regulated by 57.0% (P < 0.01). PROM1 protein and mRNA expressions were significantly down-regulated when miR-200b was overexpressed in the U87 cells (P < 0.05). siRNA-mediated down-regulation of PROM1 suppressed the potential of cell invasion. The invasion ability of SKOV3 cells after transfection with siRNA-PROM1 was significantly lower than that in the negative control cells (P < 0.05).

CONCLUSIONmiR-200b may suppress cell invasion by targeting PROM1 in glioma.

3' Untranslated Regions ; AC133 Antigen ; Antigens, CD ; metabolism ; Cell Line, Tumor ; Down-Regulation ; Genes, Reporter ; Genes, Tumor Suppressor ; Genetic Vectors ; Glioblastoma ; genetics ; metabolism ; Glycoproteins ; metabolism ; Humans ; Luciferases ; MicroRNAs ; metabolism ; Peptides ; metabolism ; RNA, Messenger ; RNA, Small Interfering ; Transfection

OBJECTIVETo elucidate whether miR-216b suppresses cell proliferation and invasion by targeting PKCα, thus to reveal the molecular mechanism that miR-216b functions as a tumor suppressor in nasopharyngeal carcinoma (NPC).

METHODSPKCα 3'UTR-luciferase vector was constructed and dual-luciferase reporter gene assay was employed to examine the effect of miR-216b on luciferase activity. Nasopharyngeal cancer CNE2 cells were transfected with miR-216b mimics, and then qRT-PCR and Western blotting were performed to detect the expressions of PKCa mRNA and protein. The effects of PKCα downregulation on cell proliferation and invasion were assessed after PKCα siRNA were transfected into CNE2 cells. CNE2 cells were cotransfected with miR-216b mimics and PKCα plasmid, and the proliferation of CNE2 cells was assayed using a MTS cell proliferation assay kit.

RESULTSThe results of dual-luciferase reporter gene assay demonstrated that miR-216b could bind to the 3'-untranslated region (UTR) of PKCα and inhibited the luciferase activity to 62.4% of that of the mimics control cells. The expressions of PKCα mRNA and protein were significantly down-regulated by 49.1% and 55.7%, respectively, in comparison with that of the control cells. siRNA-mediated downregulation of PKCα suppressed the proliferation and invasion ability of CNE2 cells, and could partially mimic the tumor-inhibiting effect of miR-216b. Moreover, the overexpressed PKCα may partially reverse the inhibitory effect of miR-216b on proliferation of CNE2 cells.

CONCLUSIONmiR-216b suppresses cell proliferation and invasion by targeting PKCα in NPC cells.

3' Untranslated Regions ; genetics ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Genetic Vectors ; Humans ; Luciferases ; genetics ; MicroRNAs ; genetics ; Nasopharyngeal Neoplasms ; genetics ; metabolism ; pathology ; Neoplasm Invasiveness ; Plasmids ; Protein Kinase C-alpha ; genetics ; metabolism ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; genetics ; Transfection

3' Untranslated Regions ; Animals ; Antagomirs ; metabolism ; Base Sequence ; Binding Sites ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Humans ; Mice ; MicroRNAs ; antagonists & inhibitors ; genetics ; metabolism ; RNA Interference ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; metabolism ; Rats ; Sequence Alignment ; Snail Family Transcription Factors ; antagonists & inhibitors ; genetics ; metabolism ; Stomach Neoplasms ; genetics ; pathology

Osteosarcoma is the most common primary sarcoma of bone, and it is a leading cause of cancer death among adolescents and young adults. However, the molecular mechanism underlying osteosarcoma carcinogenesis remains poorly understood. Recently, cyclin-dependent kinase 6 (CDK6) was identified as an important oncogene. We found that CDK6 protein level, rather than CDK6 mRNA level, is much higher in osteosarcoma tissues than in normal adjacent tissues, which indicates a post-transcriptional mechanism involved in CDK6 regulation in osteosarcoma. MiRNAs are small non-coding RNAs that repress gene expression at the post-transcriptional level and have widely been shown to play important roles in many human cancers. In this study, we investigated the role of miR-29b as a novel regulator of CDK6 using bioinformatics methods. We demonstrated that CDK6 can be downregulated by miR-29b via binding to the 3'-UTR region in osteosarcoma cells. Furthermore, we identified an inverse correlation between miR-29b and CDK6 protein levels in osteosarcoma tissues. Finally, we examined the function of miR-29b-driven repression of CDK6 expression in osteosarcoma cells. The results revealed that miR-29b acts as a tumor suppressor of osteosarcoma by targeting CDK6 in the proliferation and migration processes. Taken together, our results highlight an important role for miR-29b in the regulation of CDK6 in osteosarcoma and may open new avenues for future osteosarcoma therapies.
3' Untranslated Regions ; Animals ; Base Sequence ; Bone Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cyclin-Dependent Kinase 6 ; antagonists & inhibitors ; genetics ; metabolism ; Humans ; Mice ; MicroRNAs ; metabolism ; Osteosarcoma ; metabolism ; pathology ; RNA Interference ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; metabolism ; Rats ; Sequence Alignment ; Up-Regulation