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简介：Longnon-codingRNAs(lncRNAs)refertoagroupofRNAsthatareusuallymorethan200nucleotidesandarenotinvolvedinproteingeneration.Instead,lncRNAsareinvolvedindifferentregulatoryprocesses,suchasregulationofgeneexpression.DifferentlncRNAsexistthroughoutthegenome.LncRNAsarealsoknownfortheirrolesindifferenthumandiseasessuchascancer.HOTAIRisanlncRNAthatplaysaroleasanoncogenicmoleculeindifferentcancercells,suchasbreast,gastric,colorectal,andcervicalcancercells.Therefore,HOTAIRexpressionlevelisapotentialbiomarkerfordiagnosticandtherapeuticpurposesinseveralcancers.ThisRNAtakespartinepigeneticregulationofgenesandplaysanimportantroleindifferentcellularpathwaysbyinteractingwithPolycombRepressiveComplex2(PRC2).Inthisreview,wedescribethemolecularfunctionandregulationofHOTAIRanditsroleindifferenttypesofcancers.

简介：AbstractBackground:Rectal cancer (RC) is a malignant tumor that seriously threatens human health. Long non-coding RNAs (lncRNAs) play a vital role in tumor regulation. Nevertheless, their exact expression features and functions remain obscure, and therefore was the aim of the current study.Methods:We utilized the Affymetrix human GeneChip to screen differentially expressed profiles of lncRNAs and mRNAs from the cancer tissues and matched paracancer tissues of 6 RC patients. Gene Ontology (GO) and pathway enrichment analyses identified crucial functions and pathways of the aberrantly expressed mRNAs. We used quantitative real-time polymerase chain reaction to verify the significant expression differences of 11 candidate lncRNAs between the cancer and paracancer tissues. LncRNA-mRNA coexpression networks were built by calculating the Pearson correlation value to identify significant correlation pairs. Online bioinformatics tools GEPIA2, ONCOMINE, and PROGgeneV2 were used to mine the expression and prognosis of three crucial mRNAs and six verified lncRNAs. Competing endogenous RNA networks were constructed by predicting microRNA response elements and calculating free energy.Results:We found 1658 differentially expressed lncRNAs (778 up-regulated and 880 down-regulated) and 1783 aberrantly expressed mRNAs (909 up-regulated and 874 down-regulated). GO and pathway enrichment analyses revealed the vital functions of the differentially expressed mRNAs, including cell proliferation, cell migration, angiogenesis, and cellular response to zinc ion. The canonical signaling pathways mainly included the interleukin-17, cell cycle, Wnt, and mineral absorption signaling pathways. Six lncRNAs including AC017002.2 (P= 0.039), cancer susceptibility 19 (CASC19) (P= 0.021), LINC00152 (P= 0.013), NONHSAT058834 (P= 0.007), NONHSAT007692 (P= 0.045), and ENST00000415991.1 (P= 0.045) showed significant differences in expression levels between the cancer tissue and paracancer tissue groups. AC017002.2, NONHSAT058834, NONHSAT007692, and ENST00000415991.1 have not yet been reported in RC. The crucial mRNAs myelocytomatosis viral oncogene (MYC), transforming growth factor beta induced (TGFBI), and solute carrier family 7 member 5 (SLC7A5) were selected. AC017002.2 and LINC00152 were positively correlated with MYC, TGFBI, and cytochrome P450 family 2 sub-family B member 6 (All r > 0.900, P < 0.050). NONHSAT058834 was positively associated with MYC (r = 0.930, P < 0.001), and CASC19 was positively correlated with SLC7A5 (r= 0.922, P < 0.001).Conclusion:This study offers convincing evidence of differentially expressed lncRNAs and mRNAs as potential biomarkers in RC.

简介：AbstractBackground:Pancreatic cancer (PC) is a highly deadly malignancy with few effective therapies. We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p).Methods:SNHG6 expression was predicted by bioinformatics, followed by verification via reverse transcription quantitative polymerase chain reaction. Then, the interactions among SNHG6, miR-26a-5p, and FUBP1 were detected through online software analysis, dual luciferase reporter assay and RNA pull-down. After that, cells were treated with different small interfering RNAs and/or mimic to determine the interactions among SNHG6, miR-26a-5p, and FUBP1 and their roles in PC cells. Finally, the role of SNHG6 in tumor growth in vivo was evaluated by measuring the growth and weight of transplanted tumors in nude mice. A t-test, one-way and two-way analysis of variance were used for data analysis.Results:Compared with that in normal tissues, SNHG6 was highly expressed in PC tissues (1.00 ± 0.05 vs. 1.56 ± 0.06, t= 16.03, P < 0.001). Compared with that in human pancreatic duct epithelial cells (HPDE6-C7), SNHG6 showed the highest expression in PANC-1 cells (1.00 ± 0.06 vs. 3.87 ± 0.13, t= 34.72, P < 0.001) and the lowest expression in human pancreatic cancer cells (MIAPaCa-2) (1.00 ± 0.06 vs. 1.41 ± 0.07, t= 7.70, P= 0.0015). Compared with the levels in the si-negative control group, SNHG6 (0.97 ± 0.05 vs. 0.21 ± 0.06, t = 16.85, P < 0.001), N-cadherin (0.74 ± 0.05 vs. 0.41 ± 0.04, t= 8.93, P < 0.001), Vimentin (0.55 ± 0.04 vs. 0.25 ± 0.03, t= 10.39, P < 0.001), and β-catenin (0.62 ± 0.05 vs . 0.32 ± 0.03, t= 8.91, P < 0.001) were decreased, while E-cadherin (0.65 ± 0.06 vs. 1.36 ± 0.07, t= 13.34, P < 0.001) was increased after SNHG6 knockdown or miR-26a-5p overexpression, accompanied by inhibited cell proliferation, migration, and invasion. SNHG6 overexpression exerted the opposite effects. SNHG6 upregulated FUBP1 expression by sponging miR-26a-5p. Silencing SNHG6 blocked the growth of PC in vivo.Conclusion:Silencing SNHG6 might ameliorate PC through inhibition of FUBP1 by sponging miR-26a-5p, thus providing further supporting evidence for its use in PC treatment.

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简介：AbstractBackground:Glioblastoma is one of the most common malignant brain tumors. Conventional clinical treatment of glioblastoma is not sufficient, and the molecular mechanism underlying the initiation and development of this disease remains unclear. Our study aimed to explore the expression and function of miR-873a-5p in glioblastoma and related molecular mechanism.Methods:We analyzed the most dysregulated microRNAs from the Gene Expression Omnibus (GEO) database and examined the expression of miR-873-5p in 20 glioblastoma tissues compared with ten normal brain tissues collected in the Zhejiang Tongde Hospital. We then overexpressed or inhibited miR-873-5p expression in U87 glioblastoma cell lines and analyzed the phenotype using the cell counting kit-8 assay, wound healing assay, and apoptosis. In addition, we predicted upstream and downstream genes of miR-873-5p in glioblastoma using bioinformatics analysis and tested our hypothesis in U87 cells using the luciferase reporter gene assay and Western blotting assay. The differences between two groups were analyzed by Student’s t test. The Kruskal-Wallis test was used for the comparison of multiple groups. A P < 0.05 was considered to be significant.Results:The miR-873-5p was downregulated in glioblastoma tissues compared with that in normal brain tissues (normal vs. tumor, 0.762 ± 0.231 vs. 0.378 ± 0.114, t= 4.540, P < 0.01). Overexpression of miR-873-5p inhibited cell growth (t= 6.095, P < 0.01) and migration (t= 3.142, P < 0.01) and promoted cell apoptosis (t= 4.861, P < 0.01), while inhibition of miR-873-5p had the opposite effect. Mechanistically, the long non-coding RNA HOTAIRM1 was found to act as a sponge of miR-873-5p to activate ZEB2 expression in U87 cells.Conclusions:We uncovered a novel HOTAIRM1/miR-873-5p/ZEB2 axis in glioblastoma cells, providing new insight into glioblastoma progression and a theoretical basis for the treatment of glioblastoma.

简介：AbstractIncreasing evidence suggests that long non-coding RNAs (lncRNAs) are of vital importance for various biological processes, and dysregulation of lncRNAs is frequently associated with various diseases such as psoriasis. LncRNAs modulate gene expression at the transcriptional, post-transcriptional, and translational levels; however, the specific regulatory mechanisms of lncRNAs in psoriasis remain largely unexplored. This review provides an overview of recent studies investigating mechanisms and functions of lncRNAs in psoriasis, especially focusing on the role of lncRNAs in keratinocytes, T cells, and dendritic cells.

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简介：AbstractEndometriosis (EM) is a benign gynecological disease that affects the fertility and health of women of reproductive age; it is characterized by the presence of endometrial glands and stroma outside the uterine cavity. Although several hypotheses have been proposed to explain the underlying cause of EM, its pathogenesis remains obscure. Recently, non-coding RNAs were reported to be involved in the occurrence and development of EM. MicroRNAs and long non-coding RNAs are the main members of the non-coding RNA family that contribute to EM progression in various aspects, such as cell proliferation, apoptosis, invasion, and angiogenesis. Angiogenesis plays a pivotal role in the initiation and development of EM and provides a substantial background for the invasion, proliferation, and long-term growth of endometriotic implants. This review aimed to investigate the role of microRNAs and long non-coding RNAs in regulating angiogenesis in EM and discuss how this mechanism can be used for diagnostic and therapeutic purposes in EM.

简介：AbstractLong non-coding RNA (lncRNA) plays a contributory role in rheumatoid arthritis (RA). In this review, we summarized the current findings of lncRNAs in RA, including cellular function and the potential mechanisms. Serum lncRNA levels are associated with serum proinflammatory cytokines and disease activity. LncRNAs regulate proliferation, migration, invasion and apoptosis of RA fibroblast-like synoviocytes (FLSs), modulate the differentiation of T lymphocytes and macrophages, and affect bone formationdestruction balance of chondrocytes. Besides, lncRNAs are involved in inflammation and cell motivation signaling pathways. Indepth research on lncRNAs may help elucidate the pathogenesis of RA and provides clues for novel treatment targets.

简介：AbstractBackground:The CHA2DS2–VASc score was initially applied to stratify stroke risk in patients with atrial fibrillation (AF) and was found to be effective in predicting all-cause mortality outcomes. To date, it is still unclear whether circulating long non-coding RNAs (lncRNAs) as emerging biomarkers, can improve the predictive power of the CHA2DS2–VASc score in stroke and all-cause mortality.Methods:Candidate lncRNAs were screened by searching the literature and analyzing previous RNA sequencing results. After preliminary verification in 29 patients with AF, the final selected lncRNAs were evaluated by Cox proportional hazards regression in 192 patients to determine whether their relative expression levels were associated with stroke and all-cause mortality. The c-statistic, net reclassification improvement (NRI), and integrated discrimination improvement of the patients were calculated to evaluate the discrimination and reclassification power for stroke and all-cause mortality when adding lncRNA expression levels to the CHA2DS2–VASc score model.Results:Five plasma lncRNAs associated with stroke and all-cause mortality in AF patients were selected in our screening process. Patients with elevated H19 levels were found to have a higher risk of stroke (hazard ratio [HR] 3.264, 95% confidence interval [CI]: 1.364–7.813, P = 0.008). Adding the H19 expression level to the CHA2DS2–VASc score significantly improved the discrimination and reclassification power of the CHA2DS2–VASc score for stroke in AF patients. In addition, the H19 level showed a marginally significant association with all-cause mortality (HR 2.263, 95% CI: 0.889–5.760, P = 0.087), although it appeared to have no significant improvement for the CHA2DS2–VASc model for predicting all-cause mortality.Conclusions:Plasma expression of H19 was associated with stroke risk in AF patients and improved the discriminatory power of the CHA2DS2–VASc score. Therefore, lncRNA H19 served as an emerging non-invasive biomarker for stroke risk prediction in patients with AF.

简介：AbstractLong noncoding RNAs (lncRNAs) have recently been discovered and are increasingly recognized as vital components of modern molecular biology. Accumulating evidence shows that lncRNAs have emerged as important mediators in diverse biological processes such as cell differentiation, pluripotency, and tumorigenesis, while the function of lncRNAs in the field of normal and malignant hematopoiesis remains to be further elucidated. Here, we widely reviewed recent advances and summarize the characteristics and basic mechanisms of lncRNAs and keep abreast of developments of lncRNAs within the field of normal and malignant hematopoiesis. Based on gene regulatory networks at different levels of lncRNAs participation, lncRNAs have been shown to regulate gene expression from epigenetics, transcription and post transcription. The expression of lncRNAs is highly cell-specific and critical for the development and activation of hematopoiesis. Moreover, we also summarized the role of lncRNAs involved in hematological malignancies in recent years. LncRNAs have been found to play an emerging role in normal and malignant hematopoiesis, which may provide novel ideas for the diagnosis and therapeutic targets of hematological diseases in the foreseeable future.

简介：AbstractBackground:Long non-coding RNAs (lncRNAs) play key roles in human cancers. In our previous study, we demonstrated that lncRNA FKBP prolyl isomerase 9 pseudogene 1 (FKBP9P1) was highly expressed in head and neck squamous cell cancer (HNSCC) tissues. However, its functional significance remains poorly understood. In the present study, we identify the role and potential molecular biologic mechanisms of FKBP9P1 in HNSCC.Methods:Quantitative real-time polymerase chain reaction was used to detect the expression of FKBP9P1 in HNSCC tissues, matched adjacent normal tissues, human HNSCC cells (FaDu, Cal-27, SCC4, and SCC9), and human immortalized keratinocytes cell HaCaT (normal control). Cal-27 and SCC9 cells were transfected with sh-FKBP9P1-1, sh-FKBP9P1-2, and normal control (sh-NC) lentivirus. Cell counting kit-8 assay, colony formation assay, wound healing assay, and trans-well assay were used to explore the biologic function of FKBP9P1 in HNSCC cells. Furthermore, western blotting was used to determine the mechanism of FKBP9P1 in HNSCC progression. Chi-squared test was performed to assess the clinical significance among FKBP9P1 high-expression and low-expression groups. Survival analyses were performed using the Kaplan-Meier method and assessed using the log-rank test. The comparison between two groups was analyzed by Student t test, and comparisons among multiple samples were performed by one-way analysis of variance and a Bonferroni post hoc test.Results:FKBP9P1 expression was significantly up-regulated in HNSCC tissues (tumor vs. normal, 1.914 vs. 0.957, t = 7.746, P < 0.001) and cell lines (P < 0.01 in all HNSCC cell lines). Besides, the median FKBP9P1 expression of HNSCC tissues (1.677) was considered as the threshold. High FKBP9P1 level was correlated with advanced T stage (P = 0.022), advanced N stage (P = 0.036), advanced clinical stage (P = 0.018), and poor prognosis of HNSCC patients (overall survival, P = 0.002 and disease-free survival, P < 0.001). Knockdown of FKBP9P1 led to marked repression in proliferation, migration, and invasion of HNSCC cells in vitro (P all < 0.01). Mechanistically, silencing FKBP9P1 was observed to restrain the PI3K/AKT signaling pathway.Conclusions:Silencing lncRNA FKBP9P1 represses HNSCC progression and inhibits PI3K/AKT (phosphatidylinositol 3 kinase/AKT Serine/Threonine Kinase) signaling in vitro. Therefore, FKBP9P1 could be a potential new target for the diagnosis and treatment of HNSCC patients.

简介：AbstractBackground:Single-nucleotide polymorphisms (SNPs)-associated genes and long non-coding RNAs (lncRNAs) can contribute to human disease. To comprehensively investigate the contribution of lncRNAs to breast cancer, we performed the first genome-wide lncRNA association study on Han Chinese women.Methods:We designed an lncRNA array containing >800,000 SNPs, which was incorporated into a 96-array plate by Affymetrix (CapitalBio Technology, China). Subsequently, we performed a two-stage genome-wide lncRNA association study on Han Chinese women covering 11,942 individuals (5634 breast cancer patients and 6308 healthy controls). Additionally, in vitro gain or loss of function strategies were performed to clarify the function of a novel SNP-associated gene.Results:We identified a novel breast cancer-associated susceptibility SNP, rs11066150 (Pmeta = 2.34 × 10-8), and a previously reported SNP, rs9397435 (Pmeta= 4.32 × 10-38), in Han Chinese women. rs11066150 is located in NONHSAT164009.1 (lncHSAT164), which is highly expressed in breast cancer tissues and cell lines. lncHSAT164 overexpression promoted colony formation, whereas lncHSAT164 knockdown promoted cell apoptosis and reduced colony formation by regulating the cell cycle.Conclusions:Based on our lncRNA array, we identified a novel breast cancer-associated lncRNA and found that lncHSAT164 may contribute to breast cancer by regulating the cell cycle. These findings suggest a potential therapeutic target in breast cancer.

简介：AbstractObjective:The study aimed to detect and analyze long non-coding RNAs (lncRNAs) in plasma of children diagnosed with chronic gastritis, and to explore its biological functions and involved signaling pathways.Methods:The plasma samples were collected from six children that were diagnosed with chronic gastritis by physical examination, gastroscopy, and pathological examination and six healthy children. The plasma samples were assayed for determining the expression profiles of lncRNA based upon the gen chip detection. The specific expression of lcnRNA in plasma of children with chronic gastritis was analyzed and its biological functions were speculated.Results:Five lncRNAs (RP11-697M17.1, RP11-388M20.9, AFAP1-AS1, BC062758, and XLOC001406) were significantly upregulated, and five lncRNAs (UNQ697, BX571672.5, CYP4F35P, ANKRD20A5P, and AL832737) were observed to be significantly down-regulated. The lncRNAs RP11-697M17.1, and UNQ697 were detected with the highest up-regulation and down-regulation, respectively. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed that the up-regulated lncRNAs were significantly enriched in 20 signaling pathways such as phosphoinositide-3-kinase-protein kinase B (PI3K-Akt) pathway, and the down-regulated lncRNAs target genes were significantly enriched in 20 signaling pathways such as the metabolic pathway.Conclusion:The analysis of the lncRNA expression profiles in plasma of children with chronic gastritis revealed that the lncRNA RP11-697M17.1, and lncRNA UNQ697 may act as plasma markers for predicting chronic gastritis in children.

简介：AbstractBackground:Myocardial infarction occurs due to insufficient (ischemia) blood supply to heart for long time; plasmacytoma variant translocation 1 (PVT1) is a long non-coding RNAs (lncRNAs) involved in the pathogenesis of various diseases, including heart disease; However, few studies have explored its role. The present study evaluated the effects of lncRNA PVT1 on hypoxic rat H9c2 cells.Methods:Hypoxic injury was examined by measuring cell viability and apoptosis by using cell counting kit-8 activity and flow cytometry assays. Gene expressions after hypoxia were estimated by quantitative real time polymerase chain reaction and the signaling pathway were explored by Western blot analysis. RNA immunoprecipitation and luciferase reporter assays were applied to examine the interactions among genes. Data were analyzed using t-test with one-way or two-way analysis of variance.Results:The lncRNA PVT1 is up-regulated in hypoxia-stressed H9c2 cells and knockdown of PVT1 mitigates hypoxia-induced injury in H9c2 cells. PVT1 acts as a sponge for miR-135a-5p and knockdown of PVT1 attenuated the increased hypoxia-induced injury by up-regulating miR-135a-5p. Forkhead box O1 (FOXO1) was identified as a target of miR-135a-5p, and the expression was negatively regulated by miR-135a-5p. The exploration of the underlying mechanism demonstrated that knockdown of FOXO1 reversed PVT1/miR-135a-5p mediated hypoxia-induced injury in H9c2 cells.Conclusions:PVT1 plays a crucial role in hypoxia-injured H9c2 cells through sponging miR-135a-5p and then positively regulating FOXO1.

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简介：AIM:Toinvestigatetheeffectsofc-mybantisenseRNAoncellproliferationandtheexpressionofc-myb,TGF-β1andα1-Ⅰcollageninculturedhepaticstellatecells(HSC)fromrats.METHODS:Recombinantretroviralvectorofc-mybantisensegene(pDOR-myb)wasconstructed,andthentransfectedintoretroviralpackagecelllinePA317bymeansofDOTAP.ThepseudovirusesproducedfromtheresistantPA317cellswereselectedwithG418toinfectHSCsisolatedfromratlivers.Thecellproliferationwasmeasuredby3-[4,5-Dimethylthiazolzyl]-2,5-diphenyltetrazo-diumbromide(MTT)method.Theexpressionofc-myb,α1-ⅠcollagenandTGF-β1rnRNA,andc-mybproteininHSCswasdetectedwithsemi-quantitivereversetranseription-polymerasechainreaction(RT-PCR)andWestern-blotrespectively.RESULTS:HSCsfromratswereisolatedsuccessfullywiththeviability>98%.InthepDOR-mybinfectedHSCs,thecmybproteinexpression,cellproliferation,andα1-ⅠcollagenandTGF-β1mRNAexpressionwererepressedsignificantlycomparedwiththeircorrespondingcontrolgroups(P<0.01).CONCLUSION:c-mybplaysakeyroleinactivationandproliferationofHSC.c-mybantisenseRNAcaninhibitcellproliferation,α1-ⅠcollagenandTGF-β1mRNAexpression,suggestingthatinhibitionofc-mybgeneexpressionmightbeapotentialwayforthetreatmentofliverfibrosis.