Long Noncoding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells
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Abstract:
Glioma is the most common and lethal malignant intracranial tumor. Long noncoding RNAs (lncRNAs) have been identified as pivotal regulators in the tumorigenesis of glioma. However, the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in glioma genesis is still unknown. The purpose of this study was to investigate the underlying function of UCA1 on glioma genesis. The results demonstrated that UCA1 was upregulated in glioma tissue and indicated a poor prognosis. UCA1 knockdown induced by si-UCA1 significantly suppressed the proliferative, migrative, and invasive activities of glioma cell lines (U87 and U251). Bioinformatics analysis and luciferase reporter assay verified the complementary binding within UCA1 and miR-122 at the 3′-UTR. Functional experiments revealed that UCA1 acted as an miR-122 “sponge” to modulate glioma cell proliferation, migration, and invasion via downregulation of miR-122. Overall, the present study demonstrated that lncRNA UCA1 acts as an endogenous sponge of miR-122 to promote glioma cell proliferation, migration, and invasion, which provides a novel insight and therapeutic target in the tumorigenesis of glioma. An erratum for this article has been published in Oncology Research, Volume 28, Number 6, pp.683-684 (https://www.ingentaconnect.com/contentone/cog/or/2021/00000028/00000006/art00011). Note that an updated article PDF will be delivered from this page further to the issuing of the erratum.Keywords:
Competing Endogenous RNA
Purpose The purpose of this study was to detect the expression pattern of SPZ1 in glioma samples and to clarify its biological functions in the malignant progression of glioma. Our results provide a novel molecular target for glioma. Methods SPZ1 levels in 40 pairs of glioma and non-tumoral ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The differences in clinical indicators and prognosis between glioma patients expressing high and low levels of SPZ1 were compared. After knockdown of SPZ1 by transfection of sh-SPZ1, migratory and invasive abilities of A172 and U251 cells were examined by transwell migration and invasion assays. The interaction between SPZ1 and its target gene CXXC4 was finally explored by Western blot and dual-luciferase reporter assay. Results SPZ1 was upregulated in glioma tissues than non-tumoral ones, and the difference was statistically significant. Cell function experiments showed that knockdown of SPZ1 weakened the migratory and invasive abilities of A172 and U251 cells. CXXC4 was identified as the target gene binding to SPZ1. Knockdown of CXXC4 abolished the role of SPZ1 knockdown in inhibiting glioma progression. Conclusions SPZ1 stimulates glioma's malignant progression via targeting CXXC4.
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Long non-coding RNA colon cancer-associated transcript 2 (CCAT2) is commonly investigated in a number of cancers. However, little is known of its expression and biological function in glioma biology. In the current study, we used quantitative real-time PCR (qRT-PCR) to determine the expression of CCAT2 in glioma tissues. We found that expression of CCAT2 was up-regulated in glioma tissues and significantly correlated with the advanced tumor stage (III/IV). Functional assays in vitro and in vivo demonstrated that knockdown of CCAT2 could inhibit proliferation, cell cycle progression and migration of glioma cells. Further analysis indicated the effect of CCAT2 knockdown on glioma cell phenotype through inhibiting Wnt/β-catenin signal pathway activity. Thus, our study provides evidence that CCAT2 may function as a potential biomarker for glioma.
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BACKGROUND:A variety of treatment strategies have been developed for clear cell kidney carcinoma (KIRC); however, there is still a need for effective therapeutic targets and prognostic molecular biomarkers. Given that long noncoding RNAs (lncRNAs) has been emerging as an important regulator in tumorigenesis, we explored potential functional lncRNAs in KIRC by comprehensively analyzing the lncRNA–miRNA–mRNA regulatory network with bioinformatics processing tools. MATERIAL AND METHODS:RNA-seq/miRNA-seq data of KIRC in The Cancer Genome Atlas (TCGA) were obtained and analyzed. The “edgeR” package in R software was used to identify differentially expressed lncRNAs (DElncRNAs, differentially expressed long noncoding RNAs), miRNAs (DEmiRNAs, differentially expressed micro RNAs), and mRNAs (DEmRNAs, differentially expressed messenger RNAs) in KIRC and normal samples. A global triple network was conducted based on the competing endogenous RNA (ceRNA) theory, and survival analysis was conducted by “survival” package in R software. RESULTS:A total of 4246 DElncRNAs, 179 DEmiRNAs, and 5758 DEmRNAs were identified, among which a subset of them (321 lncRNAs, 26 miRNAs, and 1068 mRNAs) were found to constitute a global ceRNA network in KIRC. Four lncRNAs (ENTPD3-AS1, FGD5-AS1, LIFR-AS1, and UBAC2-AS1) were revealed to be potential therapeutic targets as well as prognostic biomarkers of KIRC by our extensive functional analysis. CONCLUSIONS:We reported here the identification of functional lncRNAs in KIRC via a TCGA data-based bioinformatics analysis. We believe that this study might contribute to improving the comprehension of the lncRNA-mediated ceRNA regulatory mechanisms in the tumorigenesis of KIRC. Meanwhile, our results suggested that 4 lncRNAs might act as potential therapeutic targets or candidate prognostic biomarkers in KIRC.
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Recently, long noncoding RNAs (lncRNAs) have emerged as new gene regulators and prognostic markers in several cancers, including glioma. Here we focused on lncRNA LUCAT1 on the progression of glioma. qRT-PCR was used to determine the expression of LUCAT1 and miR-375 in glioma tissues and cells. MTT and Transwell invasion assays were performed to determine the function of LUCAT1 in glioma progression. The bioinformatics tool DIANA was used to predict the targets of LUCAT1. Pearson’s correlation analysis was performed to explore the correlation between LUCAT1 and miR-375. In the present study, we showed that LUCAT1 was substantially upregulated in glioma tissues and cells. LUCAT1 inhibition significantly suppressed the proliferation and invasion of glioma cells. Subsequently, DIANA showed that miR-375 was predicted to contain the complementary binding sites to LUCAT1. Luciferase reporter assay showed that miR-375 directly targeted LUCAT1. In addition, we found that miR-375 was downregulated in glioma tissues and negatively correlated with LUCAT1 expression in glioma tissues. Furthermore, the results showed that miR-375 could rescue the function of LUCAT1 in glioma progression. The lncRNA LUCAT1 was critical for the proliferation and invasion of glioma cells by regulating miR-375. Our findings indicated that LUCAT1 might offer a potential novel therapeutic target for the treatment of glioma.
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The purpose of this study was to detect the expression pattern of SPZ1 in glioma samples and to clarify its biological functions in the malignant progression of glioma. Our results provide a novel molecular target for glioma.SPZ1 levels in 40 pairs of glioma and non-tumoral ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The differences in clinical indicators and prognosis between glioma patients expressing high and low levels of SPZ1 were compared. After knockdown of SPZ1 by transfection of sh-SPZ1, migratory and invasive abilities of A172 and U251 cells were examined by transwell migration and invasion assays. The interaction between SPZ1 and its target gene CXXC4 was finally explored by Western blot and dual-luciferase reporter assay.SPZ1 was upregulated in glioma tissues than non-tumoral ones, and the difference was statistically significant. Cell function experiments showed that knockdown of SPZ1 weakened the migratory and invasive abilities of A172 and U251 cells. CXXC4 was identified as the target gene binding to SPZ1. Knockdown of CXXC4 abolished the role of SPZ1 knockdown in inhibiting glioma progression.SPZ1 stimulates glioma's malignant progression via targeting CXXC4.
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The long non-coding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1), belongs to cancer-related lncRNAs implicated in various carcinomas, including colorectal and gastric cancers. Nonetheless, the role and underlying mechanisms of UCA1 in retinoblastoma are still unclear. This study found that UCA1 expression in retinoblastoma tissues and cells was dramatically upregulated relative to that of healthy controls. Functionally, UCA1 knockdown could suppress retinoblastoma cells' proliferation, migration and invasion, and facilitate their apoptosis. Knockdown of UCA1 also retarded the growth of xenograft tumors in vivo. Mechanistically, UCA1 promoted c-myc expression through sponging miR-124. miR-124 inhibition or c-myc overexpression partially reversed the effects of UCA1 knockdown on retinoblastoma cells. Overall, lncRNA UCA1 may exert an oncogenic effect on retinoblastoma progression through the miR-124/c-myc axis, which might serve as a promising retinoblastoma treatment target.
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Abstract Recent evidence highlights the crucial regulatory roles of long noncoding RNAs (lncRNA) in tumor biology. In colorectal cancer (CRC), the expression of several lncRNAs is dysregulated and play essential roles in CRC tumorigenesis. However, the potential biological roles and regulatory mechanisms of the novel human lncRNA, CASC2 (cancer susceptibility candidate 2), in tumor biology are poorly understood. In this study, CASC2 expression was significantly decreased in CRC tissues and CRC cell lines, and decreased expression was significantly more frequent in patients with advanced tumor-node-metastasis stage disease (TNM III and IV) ( P = 0.028). Further functional experiments indicate that CASC2 could directly upregulate PIAS3 expression by functioning as a competing endogenous RNA (ceRNA) for miR-18a. This interactions leads to the de-repression of genes downstream of STAT3 and consequentially inhibition of CRC cell proliferation and tumor growth in vitro and in vivo by extending the G 0 /G 1 -S phase transition. Taken together, these observations suggest CASC2 as a ceRNA plays an important role in CRC pathogenesis and may serve as a potential target for cancer diagnosis and treatment.
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Aim: To analyze the expression profile and competing endogenous RNA (ceRNA) network of long noncoding RNAs (lncRNAs) in nonobstructive azoospermia (NOA). Materials & methods: The lncRNA expression profile in NOA was determined by microarray reanalysis. Differential expression analysis was performed by R software. The ceRNA network was constructed using correlation analysis and gene target miRNA prediction. Metascape was used for enrichment analysis. Again ceRNA network was validated by quantitative real-time PCR. Results: Many lncRNAs are differently expressed in NOA. LncRNAs might participate in spermatogenesis through ceRNA mechanism. The ceRNA network included male gamete generation and other pathways. LINC00467 in the network regulated the expression of LRGUK and TDRD6. Conclusion: LncRNAs are involved in NOA and potential biomarkers and therapeutic targets for NOA.
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