miR-6089/MYH9/β-catenin/c-Jun negative feedback loop inhibits ovarian cancer carcinogenesis and progression

Liu, Longyang; Ning, Yingxia; Yi, Jing; Ji, Yuan; Fang, Weiyi; Lin, Zhongqiu; Zeng, Zhaoyang

doi:10.1016/j.biopha.2020.109865

Cited by 45 publications

(36 citation statements)

References 54 publications

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“…RNA pull-down assays combined with MS and WB identified MHY9. In the literature, MYH9 has been described as a strong EMT inducer that promotes the progression of various cancers [33][34][35][36]. Here, our experiments confirmed that MYH9 is also expressed in RPE cells.…”

Section: Discussionsupporting

confidence: 87%

Long noncoding RNA ERLR mediates epithelial-mesenchymal transition of retinal pigment epithelial cells and promotes experimental proliferative vitreoretinopathy

Yang

Yao

et al. 2021

Cell Death Differ

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Proliferative vitreoretinopathy (PVR) is a disease that causes severe blindness and is characterized by the formation of contractile fibrotic subretinal or epiretinal membranes. The epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells is a hallmark of PVR. This work aims to examine the role of a long noncoding RNA (lncRNA) named EMT-related lncRNA in RPE (ERLR, LINC01705-201 (ENST00000438158.1)) in PVR and to explore the underlying mechanisms. In this study, we found that ERLR is upregulated in RPE cells stimulated with transforming growth factor (TGF)-β1 as detected by lncRNA microarray and RT-PCR. Further studies characterized full-length ERLR and confirmed that it is mainly expressed in the cytoplasm. In vitro, silencing ERLR in RPE cells attenuated TGF-β1-induced EMT, whereas overexpressing ERLR directly triggered EMT in RPE cells. In vivo, inhibiting ERLR in RPE cells reduced the ability of cells to induce experimental PVR. Mechanistically, chromatin immunoprecipitation (ChIP) assays indicated that the transcription factor TCF4 directly binds to the promoter region of ERLR and promotes its transcription. ERLR mediates EMT by directly binding to MYH9 protein and increasing its stability. TCF4 and MYH9 also mediate TGF-β1-induced EMT in RPE cells. Furthermore, ERLR is also significantly increased in RPE cells incubated with vitreous PVR samples. In clinical samples of PVR membranes, ERLR was detected through fluorescent in situ hybridization (FISH) and colocalized with the RPE marker pancytokeratin (pan-CK). These results indicated that lncRNA ERLR is involved in TGF-β1-induced EMT of human RPE cells and that it is involved in PVR. This finding provides new insights into the mechanism and treatment of PVR.

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Section: Discussionsupporting

confidence: 87%

Long noncoding RNA ERLR mediates epithelial-mesenchymal transition of retinal pigment epithelial cells and promotes experimental proliferative vitreoretinopathy

Yang

Yao

et al. 2021

Cell Death Differ

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“…Dysregulation of miRNAs is established to be involved in the many diseases. miR-6089 serves a tumorsuppressive miRNA in ovarian cancer, which directly targets MYH9 to inactivate the Wnt/β-catenin and its downstream EMT [17]. In our study, we proved that miR-6089 was signi cantly decreased in synovial tissues and FLS of RA patients compared with health donor.…”

Section: Discussionsupporting

confidence: 52%

MiRNA-6089 inhibits rheumatoid arthritis fibroblast-like synoviocytes proliferation and induces apoptosis by targeting CCR4

Lin

Wang

Zhang

et al. 2020

Archives of Physiology and Biochemistry

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Background: Growing data have indicated that broblast-like synoviocytes (FLS) and miRNAs are implicated in the pathogenesis of rheumatoid arthritis (RA). This study was aimed to evaluate the function of miR-6089 in the regulation of RA-FLSs. Methods: The expression of miR-6089 was measured by quantitative real time PCR (qRT-PCR). The RA-FLSs were transfected with si-CCR4 plasmids or miR-6089 mimic, and subjected to CCK-8 and ow cytometry to analyze proliferation and apoptosis. The concentrations of MMP-1, TNF-α and IL-6 in RA-FLSs supernatant were detected using ELISA. The protein expression of caspase-3,-8 and-9 was detected using western blot. Results: The levels of miR-6089 were detected to be signi cantly lower in the synovial tissues and FLSs of RA than in the synovial tissues and FLSs of healthy controls. The miR-6089 up-regulation in RA-FLSs signi cantly inhibited the proliferation and promoted cell apoptosis accompany with an increase protein expression of caspase-3,-8 and-9. Furthermore, CCR4 was determined to directly target miR-6089, and its expression was signi cantly increased in the synovial tissues of RA than in the synovial tissues of healthy controls. Moreover, CCR4 overexpression effectively reversed the effect on proliferation and apoptosis induced by miR-6089 in RA-FLSs. Conclusion: Our results revealed that miR-6089 may be a potential target for RA prevention and therapy of RA.

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“…The Wnt signaling cascade was highly conserved among species and controls a multitude of biological processes during animal development and life cycles. Because of its central role in the maintenance of tissue homeostasis, the Wnt pathway was tightly regulated at multiple levels, from the ligand-receptor interaction down to transcriptional and post-transcriptional levels; its aberrant activity has been implicated in a number of developmental disorders and diseases and, most prominently, in cancer (Nusse and Clevers, 2017;Nguyen et al, 2019;Zhang et al, 2019;Liu et al, 2020). The recent discovery of lncRNAs that are regulated by Wnt and/or participate in Wnt pathway modulation and outcome is particularly intriguing and has highlighted some of these gaps in our knowledge (Zarkou et al, 2018).…”

Section: Regulatory Mechanism Of Linc-ror In Various Types Of Cancermentioning

confidence: 99%

Relevance Function of Linc-ROR in the Pathogenesis of Cancer

Chen

Yang

Fang

et al. 2020

Front. Cell Dev. Biol.

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Long non-coding RNAs (lncRNAs) are the key components of non-coding RNAs (ncRNAs) with a length of 200 nucleotides. They are transcribed from the so-called "dark matter" of the genome. Increasing evidence have shown that lncRNAs play an important role in the pathophysiology of human diseases, particularly in the development and progression of tumors. Linc-ROR, as a new intergenic non-protein coding RNA, has been considered to be a pivotal regulatory factor that affects the occurrence and development of human tumors, including breast cancer (BC), colorectal cancer (CRC), pancreatic cancer (PC), hepatocellular carcinoma (HCC), and so on. Dysregulation of Linc-ROR has been closely related to advanced clinicopathological factors predicting a poor prognosis. Because linc-ROR can regulate cell proliferation, apoptosis, migration, and invasion, it can thus be used as a potential biomarker for patients with tumors and has potential clinical significance as a therapeutic target. This article reviewed the role of linc-ROR in the development of tumors, its related molecular mechanisms, and clinical values.

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miR-6089/MYH9/β-catenin/c-Jun negative feedback loop inhibits ovarian cancer carcinogenesis and progression

Cited by 45 publications

References 54 publications

Long noncoding RNA ERLR mediates epithelial-mesenchymal transition of retinal pigment epithelial cells and promotes experimental proliferative vitreoretinopathy

Long noncoding RNA ERLR mediates epithelial-mesenchymal transition of retinal pigment epithelial cells and promotes experimental proliferative vitreoretinopathy

MiRNA-6089 inhibits rheumatoid arthritis fibroblast-like synoviocytes proliferation and induces apoptosis by targeting CCR4

Relevance Function of Linc-ROR in the Pathogenesis of Cancer

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