Long noncoding RNA LINC00324 promotes retinoblastoma progression by acting as a competing endogenous RNA for microRNA-769-5p, thereby increasing STAT3 expression

Dong, Yi; Wan, Guangming; Yan, Panshi; Qian, Cheng; Li, Fuzhen; Peng, Guang-Hua

doi:10.18632/aging.103075

Cited by 23 publications

(26 citation statements)

References 45 publications

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“…The present study found out the miR-491-3p targeted mRNA SNN. Target site-mutated SNN did not interact with miR-491-3p in our study has confirmed our prediction, which was consistence with similar approach in other studies (Cheng et al 2019 ; Dong et al 2020 ). But there was a pity that we were unable to include SSN-MUT in the rest of our experiments certainly was an unfortunate limitation to our study that was due to time and cost constraint, but we will certainly revisit this limitation in our future study.…”

Section: Discussionsupporting

confidence: 93%

miR-491-3p is Downregulated in Retinoblastoma and Inhibit Tumor Cells Growth and Metastasis by Targeting SNN

Zhao

et al. 2020

Biochem Genet

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Retinoblastoma (Rb) is the most common pediatric malignant tumor of the eyes. Previous studies demonstrated that miR-491-3p is downregulated in various cancers. However, its function in Rb remains unknown. A total of 15 pairs of primary Rb tissues and adjacent noncancerous tissues were collected. Quantitative real-time PCR (qRT-PCR) was used to investigate the expression profiles of miR-491-3p. qRT-PCR, western blotting and in situ immunocytochemistry were performed to investigate the expression profiles of epithelial–mesenchymal transition-related proteins (E-cadherin, Vimentin and N-cadherin) in Rb tissues and Rb cell lines as well as cell morphology. Cell proliferation was estimated by MTS and colony formation assays. Apoptosis was determined by FACS, cell migration and invasion were analyzed using transwell chambers. MiR-491-3p’s target genes were predicted using target gene prediction databases. The interplay between miR-491-3p and SNN was evaluated through dual luciferase reporter gene assay. MiR-491-3p was significantly downregulated in mixed collection of 15 pairs of Rb tissues and Rb cell lines. Overexpression of miR-491-3p enhanced apoptosis, and significantly suppressed proliferation, migration and invasion of Rb cells. In contrast, the present of miR-491-3p inhibitor showed reversed results which apoptosis decreased, while cell proliferation of ARPE-19 cells increased. In addition, miR-491-3p increased the expression of E-cadherin, and dramatically decreased the expression of Vimentin and N-cadherin in Rb tissues and Rb cell lines, noticeable changes in morphology, too, as cells became less cohesive and more adhering. We found out that SNN was the pairing target of miR-491-3p and result showed that miR-491-3p and SNN interacted with each other. We also found out that the effects of miR-491-3p were in Rb cells were almost entirely canceled out at the overexpression of SNN. Our findings collectively suggest that miR-491-3p is an important tumor suppressor in Rb, which inhibits tumor growth and metastasis in Rb. These implicate it may be explored as a new therapeutic target in Rb.

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Section: Discussionsupporting

confidence: 93%

miR-491-3p is Downregulated in Retinoblastoma and Inhibit Tumor Cells Growth and Metastasis by Targeting SNN

Zhao

et al. 2020

Biochem Genet

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“…Evidences have proven that lncRNAs utilize miRNAs to exert functions and miRNAs are important regulators of tumorigenesis and invasion. 6 , 21 For example, lncRNA HOXA-AS2 sponges miR-509-3p to promote prostate cancer development. 22 LncRNA DLX6-AS1 is the decoy for miR-195-5p to aggravate ovarian cancer progression.…”

Section: Discussionmentioning

confidence: 99%

“… 5 LncRNA may exert functions through multiple kinds of manners, such as epigenetic or post-transcriptional levels. 6 LncRNA participates in the regulation of various biological processes in cancer, including proliferation, invasion, apoptosis and differentiation. 7 , 8 For instance, lncRNA DLX6-AS1 contributes to prostate cancer growth and invasion through enhancing LARGE methylation.…”

Section: Introductionmentioning

confidence: 99%

LncRNA ELFN1-AS1 Promotes Retinoblastoma Growth and Invasion via Regulating miR-4270/SBK1 Axis

Feng¹,

Zhu²,

Ma³

et al. 2021

CMAR

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Background Long noncoding RNA (lncRNA) has been reported to play important roles in tumor initiation. However, how lncRNA ELFN1-AS1 affects retinoblastoma development remains unclear. Thus, we sought to elucidate its functions in retinoblastoma progression. Methods ELFN1-AS1 expression was measured in retinoblastoma tissues and normal tissues by qRT-PCR. CCK8, colony formation and Transwell assay were carried out to investigate the effects of ELFN1-AS1 knockdown on cell malignant behaviors. Bioinformatics analyses were performed to predict the relationship among ELFN1-AS1, miR-4270 and SBK1. Results ELFN1-AS1 was highly expressed in retinoblastoma tissues and cell lines. ELFN1-AS1 was positively correlated with retinoblastoma progression and prognosis. ELFN1-AS1 knockdown curtailed retinoblastoma proliferation, migration and invasion. ELFN1-AS1 was the competing endogenous RNA for miR-4270 and promoted SBK1expression. Conclusion Altogether, our findings demonstrated that ELFN1-AS1 promotes retinoblastoma progression through mediating miR-4270/SBK1 axis and might be a promising therapeutic target.

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“…In this study, we found that miR-769-5p was a downstream target of MALAT1 and reversely modulated by MALAT1. Numerous studies indicated that miR-769-5p participates in the growth of some cancers and is reduced in non-small-cell lung carcinoma (NSCLC) [ 36 ] and retinoblastoma (RB) [ 37 ]. Interestingly, Du et al have pointed that miR-769-5p expression is decreased in LPS-treated PDLCs [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis

Chen

Cao

2021

BioMed Research International

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Purpose. Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. Methods. Primary human periodontal ligament cells (PDLCs) were treated with P. gingivalis lipopolysaccharide (LPS) to establish a CP model. Quantitative real-time PCR (qRT-PCR) was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines. The protein levels of caspase-3, Bax, Bcl-2, and hypoxia-inducible factor (HIF) 3A were determined by western blot assay. Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A. Results. The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro. Conclusion. MALAT1 knockdown attenuated LPS-induced PDLC injury via regulating the miR-769-5p/HIF3A axis, which may supply a new target for CP treatment.

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Long noncoding RNA LINC00324 promotes retinoblastoma progression by acting as a competing endogenous RNA for microRNA-769-5p, thereby increasing STAT3 expression

Cited by 23 publications

References 45 publications

miR-491-3p is Downregulated in Retinoblastoma and Inhibit Tumor Cells Growth and Metastasis by Targeting SNN

miR-491-3p is Downregulated in Retinoblastoma and Inhibit Tumor Cells Growth and Metastasis by Targeting SNN

LncRNA ELFN1-AS1 Promotes Retinoblastoma Growth and Invasion via Regulating miR-4270/SBK1 Axis

Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis

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