Long non‐coding <scp>RNA</scp>s in ocular diseases: new and potential therapeutic targets

Zhang, Lixia; Dong, Yanhan; Wang, Yujie; Gao, Jinling; Lv, Jiayi; Sun, Jialin; Li, Mengjie; Wang, Meng; Zhao, Zhihong; Wang, Jianxun; Xu, Wu

doi:10.1111/febs.14827

Cited by 51 publications

(47 citation statements)

References 79 publications

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“…The aberrantly expressed lncRNAs, which act as diagnostic markers, prognostic indicators or predictors of therapeutic response, have been reported in various types of cancer including HCC 23 , 24 . For instance, the identification of tumor-specific transcripts (TSTs), which contain many noncoding RNAs and are detectable in extracellular vesicles from HCC patients' blood, may provide new insights into the development of HCC diagnosis 25 .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis

Xiao¹,

Liu

Zhao³

et al. 2020

Int. J. Biol. Sci.

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Hepatocellular carcinoma (HCC), one of the main causes of cancer-related deaths globally, is characterized by rapid growth and high invasiveness. Accumulating evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in the growth and metastasis of HCC. Recently, lncRNA LINC01123 has been found to contribute to cell proliferation and aerobic glycolysis in lung cancer. However, the function of LINC01123 in HCC, as well as the underlying mechanism of its action, remain unclear. Here, we found that the expression of LINC01123 was clearly upregulated in HCC tissues compared to nontumor tissues. Furthermore, expression of LINC01123 in HCC cells was significantly higher than in LO2 cells. Importantly, the upregulated level of LINC01123 was related to unfavorable clinical features and poor prognosis of HCC. Next, we demonstrated that LINC01123 knockdown suppressed the proliferation, migration and invasion of HCC cells in vitro . Depletion of LINC01123 inhibited HCC xenograft growth in vivo . Conversely, ectopic expression of LINC01123 facilitated HCC cell proliferation and invasion. Mechanistically, LINC01123 acted as a molecular sponge for miR-34a-5p in HCC cells. Tuftelin1 (TUFT1) was identified as the target gene of miR-34a-5p. LINC01123 positively regulated TUFT1 level by targeting of miR-34a-5p in HCC cells. Notably, TUFT1 restoration can abolish miR-34a-5p-induced inhibitory effects on HCC cell proliferation, migration and invasion. In conclusion, LINC01123 was overexpressed in HCC and accelerated cancer cell proliferation and invasion by regulating the miR-34a-5p/TUFT1 axis.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis

Xiao¹,

Liu

Zhao³

et al. 2020

Int. J. Biol. Sci.

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“…MicroRNA-194 overexpression can also suppress RPE cell EMT by attenuating the expression of Zeb1 ( Cui et al, 2019 ). In addition to miRNAs, long non-coding RNAs (lncRNAs) contribute to the regulation of RPE EMT ( Zhang et al, 2019 ). In RPE cells treated with PVR vitreous or TGF-β1, MALAT1 expression is increased, and knockdown of MALAT1 attenuates the phosphorylation of SMAD2/3 and the expression of Snail, Slug, and Zeb1, preventing cell migration and proliferation ( Yang et al, 2016 ).…”

Section: Survey Methodologymentioning

confidence: 99%

Polarity and epithelial-mesenchymal transition of retinal pigment epithelial cells in proliferative vitreoretinopathy

Zou

Shan

et al. 2020

PeerJ

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Under physiological conditions, retinal pigment epithelium (RPE) is a cellular monolayer composed of mitotically quiescent cells. Tight junctions and adherens junctions maintain the polarity of RPE cells, and are required for cellular functions. In proliferative vitreoretinopathy (PVR), upon retinal tear, RPE cells lose cell-cell contact, undergo epithelial-mesenchymal transition (EMT), and ultimately transform into myofibroblasts, leading to the formation of fibrocellular membranes on both surfaces of the detached retina and on the posterior hyaloids, which causes tractional retinal detachment. In PVR, RPE cells are crucial contributors, and multiple signaling pathways, including the SMAD-dependent pathway, Rho pathway, MAPK pathways, Jagged/Notch pathway, and the Wnt/β-catenin pathway are activated. These pathways mediate the EMT of RPE cells, which play a key role in the pathogenesis of PVR. This review summarizes the current body of knowledge on the polarized phenotype of RPE, the role of cell-cell contact, and the molecular mechanisms underlying the RPE EMT in PVR, emphasizing key insights into potential approaches to prevent PVR.

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“…5,6 Numerous studies have demonstrated that lncRNAs play a vital role in different cellular processes, such as proliferation, differ-entiation, migration, invasion, and apoptosis, and exhibit differential expression in the pathogenesis of ophthalmologic disorders. 5,[7][8][9][10][11][12] Interestingly, some studies have suggested that the lncRNA-mRNA competitive endogenous RNA network plays a role in the transcriptional regulation of I/R injury, in which lncRNA functions as a competitive endogenous RNA (ceRNA) that competes for microRNA (miRNA) in order to increase the expression of a particular target gene. [13][14][15][16] Therefore, we hypothesized whether lncR-NAs could influence the process of apoptosis in RGCs via the ceRNA pathway in a mouse model of I/R damage.…”

mentioning

confidence: 99%

lncRNA Ttc3-209 Promotes the Apoptosis of Retinal Ganglion Cells in Retinal Ischemia Reperfusion Injury by Targeting the miR-484/Wnt8a Axis

Zhang

Feng

et al. 2021

Invest. Ophthalmol. Vis. Sci.

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Apoptosis of the retinal ganglion cells (RGCs) can cause irreversible damage to visual function after retinal ischemia reperfusion injury (RIR). Using a lncRNA chip assay, we selected lncRNA Ttc-209 and characterized its role in RGCs during ischemia reperfusion (I/R)-induced apoptosis. METHODS.We created an ischemic model of RGCs by applying Hank's balanced salt solution containing 10 μM antimycin A and 2 μM calcium ionophore for 2 hours. RIR was induced in mice by elevating the intraocular pressure to 120 mm Hg for 1 hour by cannulation of the cornea; this was followed by reperfusion. Real-time quantitative PCR was used to detect the expression levels of long noncoding RNA (lncRNA), microRNA (miRNA), and target gene mRNA. Western blotting, flow cytometry, immunofluorescent staining, and TUNEL assays were performed to detect cell apoptosis. Dual-luciferase reporter assays and FISH were used to identify endogenous competitive RNA (ceRNA) mechanisms that link lncRNAs, miRNAs, and target genes. We also used scotopic electroretinography examinations to evaluate visual function in treated mice.RESULTS. lncRNA Ttc3-209 was significantly upregulated after I/R injury and played a proapoptotic role in RGCs during I/R-induced apoptosis. Mechanistically, lncRNA Ttc3-209 is a ceRNA that competitively binds to miR-484 and upregulates the translation of its target (Wnt8a mRNA), thus promoting apoptosis in RGCs. CONCLUSIONS.Reducing the expression of lncRNA Ttc3-209 had a protective effect against apoptosis in RGCs. This may provide a new therapeutic option for the prevention of RGC apoptosis in response to RIR injury.

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Long non‐coding RNAs in ocular diseases: new and potential therapeutic targets

Cited by 51 publications

References 79 publications

Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis

Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis

Polarity and epithelial-mesenchymal transition of retinal pigment epithelial cells in proliferative vitreoretinopathy

lncRNA Ttc3-209 Promotes the Apoptosis of Retinal Ganglion Cells in Retinal Ischemia Reperfusion Injury by Targeting the miR-484/Wnt8a Axis

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