Recent studies have discovered that long noncoding RNAs (lncRNAs) play an important role in malignant tumors. In this research, lncRNA ROR1-AS1 was selected to identify how it affects the development of colorectal cancer (CRC). ROR1-AS1 expression was detected by RT-qPCR in CRC tissue samples. ROR1-AS1 expression level and patients’ overall survival time were analyzed. Functional experiments were conducted to identify the changes of biological behaviors in CRC cells after knockdown of ROR1-AS1. Moreover, we also explored the underlying mechanism. Detection of ROR1-AS1 expression level in patients’ tissues showed that ROR1-AS1 was higher in CRC tissues than that in adjacent ones. ROR1-AS1 expression was negatively associated with patients’ overall survival time. Cell growth ability was inhibited due to knockdown of ROR1-AS1 in vitro . Moreover, cell migration and invasion were repressed after ROR1-AS1 knockdown. Furthermore, due to knockdown of ROR1-AS1, the targeted proteins in Wnt/β-catenin signaling pathway were suppressed. These results suggest that ROR1-AS1 could enhance cell metastasis and proliferation via inducing Wnt/β-catenin signaling pathway, which might offer a potential therapeutic target in CRC.

Long noncoding RNAs (lncRNAs), more than 200 nt in length, are functional molecules found in various species. These lncRNAs play a vital role in cell proliferation, differentiation, and degeneration and are also involved in pathophysiological processes of cancer and neurodegenerative, autoimmune, and cardiovascular diseases (CVDs). In recent years, emerging challenges for intervention studies on ischemic heart diseases have received much attention. LncRNAs have a key function in the alleviation of myocardial infarction (MI) injury and myocardial ischemia–reperfusion injury. During cardiac hypertrophy (CH) and fibrosis, cardiac cells undergo structural changes and become dysfunctional due to the effects of neurohormonal factors. LncRNAs may serve as important therapeutic targets that promote cardiac remodeling and then retard the development of heart failure (HF). In addition, studies on the roles and mechanisms of action of lncRNAs participating in cardiac pathophysiology via other factors have become the focus of research worldwide. Here, we review the current knowledge on various lncRNAs and their functions in cardiac biology, particularly concentrating on ischemic heart disease, CH, and cardiac fibrosis. We next discuss the predictive value of lncRNAs as diagnostic biomarkers of CVDs.

Long noncoding RNA HOXB cluster antisense RNA 3 (HOXB-AS3) has been reported to be dysregulated in several tumors. The present study mainly aims at the investigation in how HOXB-AS3 works in epithelial ovarian cancer (EOC) and to elucidate the mechanism involved. Initially, ‘GEPIA’ was mined to examine the differential expression levels and prognostic value of HOXB-AS3 in EOC patients. The expression of HOXB-AS3 in EOC cell lines and patient specimens was examined with quantitative RT-PCR. Simultaneously, the correlation of HOXB-AS3 expression with a variety of clinicopathological factors and patient survival was analyzed. MTT, colony formation and flow cytometry assays were performed to analyze the cell viability of EOC cells. Wound healing and Transwell assays were carried out to determine EOC cells’ capability of migrating and invading. The impact of HOXB-AS3 on EMT and Wnt/β-catenin signaling was explored with the approach of Western blot. We found that in both EOC cell lines and tissues, HOXB-AS3 expression was significantly up-regulated, and its high expression was an independent prognostic marker of poor outcome for EOC patients. In vitro loss-of-function assays revealed that HOXB-AS3 knockdown inhibited EOC cells proliferation, migration, invasion and EMT, and induced EOC cells’ apoptosis. Furthermore, we validated that down-regulated HOXB-AS3 attenuated the activity of Wnt/β-catenin signaling to suppress the invasion, migration and proliferation of EOC cells. To sum up, the present study came up with the conclusion that HOXB-AS3 acts as an oncogenic gene in EOC progression through HOXB-AS3-Wnt/β-catenin signaling regulation, providing a novel insight into EOC tumorigenesis.

Background H19 polymorphisms have been reported to correlate with an increased susceptibility to a few types of cancers, although their role in neuroblastoma has not yet been clarified. Materials and methods We investigated the association between three single polymorphisms (rs2839698 G>A, rs3024270 C>G, and rs217727 G>A) and neuroblastoma susceptibility in Chinese Han populations. Three hundred ninety-three neuroblastoma patients and 812 healthy controls were enrolled from the Henan and Guangdong provinces. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to determine the strength of the association of interest. Results Separated and combined analyses revealed no associations of the rs2839698 G>A, rs3024270 C>G or rs217727 G>A polymorphisms and neuroblastoma susceptibility. In the stratification analysis, female children with rs3024270 GG genotypes had an increased neuroblastoma risk (adjusted OR = 1.61, 95% CI = 1.04–2.50, P =0.032). Conclusion The rs3024270 GG genotype might contribute to an increased neuroblastoma susceptibility in female Chinese children.

Background: Coronary artery disease (CAD) is one of the main fatal diseases all over the world. CAD is a complex disease, which has multiple risk factors mechanisms. In recent years, genome-wide association study (GWAS) had revealed single nucleotide polymorphism genes (SNPs) which were closely related with CAD risks. The relationship between long non-coding RNA (lncRNA) MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) and CAD risk is largely unknown. To our knowledge, this is the first study which demonstrated the interaction effects of SNP–SNP and SNP–environment with CAD risk. In general, our case–control study is to detect the association between MALAT1 (rs619586, rs4102217) SNPs and CAD risk. Methods: Three hundred and sixty-five CAD patients and three hundred and eighty-four matched control participants blood samples were collected in Liaoning province, China. Two polymorphisms (rs619586, rs4102217) in lncRNA MALAT1 were genotyped by KASP platform. Results: In a stratified analysis, we found that non-drinkers with GC genotype and the recessive model of rs4102217 had higher CAD risk ( P =0.010, odds ratio (OR): 1.96, 95% confidence interval (CI) = 1.17–3.28; P =0.026, OR: 1.73, 95% CI = 1.07–2.79) and diabetes mellitus (DM) history group ( P =0.010, OR: 4.07, 95% CI = 1.41–11.81; P =0.019, OR: 3.29, 95% CI = 1.22–8.88). In SNP–SNP interactions analysis between MALAT1 and CAD risk, we found rs4102217 had an increase in smokers (GG: OR: 2.04, 95% CI = 1.42–2.92; CC+GC: OR: 2.64, 95% CI = 1.64–4.26) and a decrease in drinkers (CC+GC: OR: 0.33, 95% CI = 0.20–0.55). Smokers with MALAT1 rs619586 AA genotype (OR: 2.20, 95% CI = 1.57–3.07) and GG+AG genotype (OR: 2.11, 95% CI = 1.17–3.81) had a higher risk of CAD. Moreover, drinkers with AA genotype (OR: 0.22, 95% CI = 0.10–0.48) and GG+AG genotype (OR: 0.38, 95% CI = 0.22–0.65) had a lower risk of CAD. According to the MDR software, MALAT1 rs4102217 polymorphism-smoking-drinking was the best interaction model, which has higher risk of CAD (Testing Bal.ACC. = 0.6979). Conclusion: Our study demonstrated that the GC genotype and the recessive model of rs4102217 potentially increased CAD risk in some specific group.

The present study was undertaken to investigate the underlying mechanisms of long noncoding RNA OIP5-AS1 via regulating miR-410 to modulate Wnt-7b in the progression of glioma. To address this problem, we measured the expression of OIP5-AS1 and miR-410 in glioma tissues by qRT-PCR. Glioma U87 cells were transfected with OIP5-AS1 siRNA or miR-410 inhibitors. The targeting relationships among miR-410, OIP5-AS1 and Wnt-7b were verified by luciferase reporter assays. Western blotting was employed to determine the expression of Wnt-7b/β-catenin pathway-related proteins, while MTT, flow cytometry, Transwell assays and wound-healing assays were used to measure the biological characteristics of glioma cells. The results showed that OIP5-AS1 expression was higher and miR-410 was lower in glioma tissues. Luciferase reporter assays confirmed a targeting relationship between OIP5-AS1 and miR-410, as well as between miR-410 and Wnt-7b. Silencing OIP5-AS1 reduced cell proliferation, invasion and migration of glioma U87 cells and led to depressed expression levels of miR-410, Wnt-7b, p-β-catenin, GSK-3β-pS9, c-Myc and cyclin D1. Furthermore, down-regulation of OIP5-AS1 induced G0/G1 phase cell cycle arrest and apoptosis of glioma cells. Inhibitors of miR-410 abolished the biological effects of OIP5-AS1 siRNA in glioma cells. In vivo , OIP5-AS1 knockdown also inhibited tumor growth. Taken together, this research suggested that silencing OIP5-AS1 may specifically block the Wnt-7b/β-catenin pathway via targeted up-regulating miR-410, thereby inhibiting growth, invasion and migration while promoting apoptosis in glioma cells.

As a kind of essential regulators, long noncoding RNAs (lncRNAs) have attracted a lot of attention in recent years. Nevertheless, the function of lncRNA in nasopharyngeal carcinoma (NPC) remains poorly understood. In the present study, we explained the role and mechanism of LINC00210 in NPC progression. We found that LINC00210 expression was up-regulated in NPC samples. Besides, its overexpression was positively correlated with NPC metastasis while predicting poor prognosis. Based on functional experiments, we revealed that LINC00210 contributed to NPC cell proliferation and invasion in vitro , and promotes tumor growth in vivo . Mechanistically, we identified that LINC00210 was located in the cytoplasm of NPC cells and served as the miR-328-5p sponge. Furthermore, we showed that miR-328-5p targets the 3′ untranslated region (3′-UTR) of NOTCH3. Through inhibiting miR-328-5p activity, LINC00210 promoted NOTCH3 expression in NPC, leading to activation of NOTCH3 signaling pathway. In conclusion, our study indicates LINC00210 promotes NPC progression through modulating proliferation and invasion.

Gastric cancer (GC) is one of the major causes of cancer deaths worldwide; however, the mechanism of carcinogenesis is complex and poorly understood. Long non-coding RNA (lncRNA) has been reported to be involved in the development of multiple cancers. Here, we identified a novel lncRNA, AK096174, which was up-regulated and associated with tumorigenesis, tumor size, metastasis, and poor prognosis in GC. Our data showed that AK096174 was highly expressed in the GC tissues and cell lines (SGC-7901, AGS, BGC-823, MGC-803), and patients with higher AK096174 expression had a poorer prognosis and shorter overall survival (OS). AK096174 knockdown inhibited the proliferation, migration, and invasiveness in SGC-7901 and BGC-823 cells, whereas AK096174 overexpression had the promoting effects. Furthermore, mechanistic investigation showed that AK096174 positively correlated with the expression of WD repeat-containing protein 66 ( WDR66 ) gene at the translational level. Knockdown of WRD66 attenuated the positive impact of AK096174 in GC cells. The findings of the present study establish a function for AK096174 in GC progression and suggest it may serve as a potential target for GC therapy in the future.

Diabetic retinopathy (DR) is the leading cause of blindness in working-age adults across the world. The pathogenesis of DR is multifactorial and the molecular mechanisms are still not fully understood. Accumulating evidence has demonstrated that noncoding RNAs (ncRNAs) may be aberrantly expressed and may play vital roles in the development of DR. Amongst ncRNAs, miRNAs and long ncRNAs (lncRNAs) are known for their regulatory functions. Here, we summarize the functions and mechanisms of known aberrantly expressed miRNAs and lncRNAs in DR. Additionally, a novel lncRNA–mRNA–miRNA network is included in this review. We highlight original studies that provide detailed data about the mechanisms of miRNAs and lncRNAs, their applications as diagnostic or prognostic biomarkers, and their potential therapeutic targets. In conclusion, this review will help us gain a better understanding of the molecular mechanisms by which miRNAs and lncRNAs perform their functions in DR, and provide general strategies and directions for future research.

Melanoma is the most malignant skin cancer, which account for most of skin-cancer-related deaths. Long noncoding RNA (lncRNA) is a class of noncoding RNAs with crucial roles in many cancers. However, the roles of lncRNAs in melanoma have not been well studied. In the present study, using public available data and clinical tissues samples, we found that lncRNA ILF3-AS1 is up-regulated in melanoma tissues and cell lines, and correlated with poor prognosis of melanoma patients. Functional experiments showed that knockdown of ILF3-AS1 inhibits melanoma cell proliferation, migration, and invasion. Mechanistically, we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues. Moreover, inhibition of miR-200b/a/429 abrogates the biological roles of ILF3-AS1 knockdown on melanoma cell proliferation, migration, and invasion. In conclusion, these results demonstrate that melanoma-upregulated lncRNA ILF3-AS1 promotes cell proliferation, migration, and invasion via negatively regulating miR-200b/a/429, and imply that ILF3-AS1 may be a potential prognostic biomarker and therapeutic target for melanoma.

Long noncoding RNAs (lncRNAs) are frequently dysregulated and have important roles in many diseases, particularly cancers. lncRNA-HEIH was first identified in hepatocellular carcinoma (HCC). The expression, clinical significance and roles of lncRNA-HEIH in melanoma are still unknown. In the present study, we found that lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription. The expression of miR-200b is inversely associated with lncRNA-HEIH in melanoma tissues. Furthermore, overexpression of miR-200b/a/429 abrogates melanoma cell proliferation, migration and invasion enhanced by lncRNA-HEIH. In conclusion, we identified lncRNA-HEIH as a key oncogene in melanoma via transcriptional inhibition of miR-200b/a/429 . Our data suggested that lncRNA-HEIH may serve as a promising prognostic biomarker and therapeutic target for melanoma.

The present study explored the effect of long non-coding RNA-human ovarian cancer-specific transcript 2 (LncRNA-HOST2) on cell proliferation, migration, invasion and apoptosis of human hepatocellular carcinoma (HCC) cell line SMMC-7721. HCC tissues and adjacent normal tissues from 162 HCC patients were collected. The HCC cell lines were assigned into the control group (regular culture), negative control (NC) group (transfected with siRNA) and experimental group (transfected with Lnc-HOST2 siRNA). Quantitative real-time PCR (qRT-PCR) was used to detect the expression of LncRNA-HOST2. Cell proliferation was detected by CCK-8 and colony-forming assays, cell apoptosis by flow cytometry and cell migration by Scratch test. Transwell assay was used to evaluate cell migration and invasion abilities. LncRNA-HOST2 expression in the HCC tissues increased 2–10 times than that in the adjacent normal tissues. Compared with the HL-7702 cell line, LncRNA-HOST2 expression in HepG2, SMMC-7721 and Huh7 cell lines was all up-regulated, but the SMMC-7721 cell had the highest Lnc-HOST2 expression. The LncRNA-HOST2 expression in the experimental group was down-regulated as compared with the control and NC groups. In comparison with the control and NC groups, cloned cells reduced, cell apoptosis increased, clone-forming ability weakened and inhibitory rate of colony formation increased in the experimental group. The cells migrating and penetrating into the transwell chamber were fewer in the experimental group than those in the control and NC groups. The experimental group exhibited slow wound healing and decreased cell migration area after 48 h. These findings indicate that LncRNA-HOST2 can promote cell proliferation, migration and invasion and inhibit cell apoptosis in human HCC cell line SMMC-7721.