Long non‐coding RNA RP11‐820 promotes extracellular matrix production via regulating miR‐3178/MYOD1 in human trabecular meshwork cells

Shen, Wencui; Huang, Bingqing; He, Ye; Shi, Liukun; Yang, Jin

doi:10.1111/febs.15058

Cited by 26 publications

(17 citation statements)

References 43 publications

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“…Increasing evidences have demonstrated that lncRNAs are involved in almost all diseases [43][44][45]. For instance, FEZF1-AS1 was revealed to be overexpressed in PDAC and promote PDAC progression and Warburg effect [27].…”

Section: Discussionmentioning

confidence: 99%

KLHDC7B-DT aggravates pancreatic ductal adenocarcinoma development via inducing cross-talk between cancer cells and macrophages

Wang

Yuan

et al. 2021

Clinical Science

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Tumor microenvironment (TME) exerts key roles in pancreatic ductal adenocarcinoma (PDAC) development. However, the factors regulating the crosstalk between PDAC cells and TME are largely unknown. In this study, we identified a long noncoding RNA (lncRNA) KLHDC7B-DT, which was upregulated in PDAC and correlated with poor survival of PDAC patients. Functional assays demonstrated that KLHDC7B-DT enhanced PDAC cell proliferation, migration, and invasion. Mechanistically, KLHDC7B-DT was found to directly bind IL-6 promoter, induce open chromatin structure at IL-6 promoter region, activate IL-6 transcription, and upregulate IL-6 expression and secretion. The expression of KLHDC7B-DT was positively correlated with IL-6 in PDAC tissues. Via inducing IL-6 secretion, KLHDC7B-DT activated STAT3 signaling in PDAC cells in an autocrine manner. Furthermore, KLHDC7B-DT also activated STAT3 signaling in macrophages in a paracrine manner, which induced macrophage M2 polarization. KLHDC7B-DT overexpressed PDAC cells-primed macrophages promoted PDAC cell proliferation, migration, and invasion. Blocking IL-6/STAT3 signaling reversed the effects of KLHDC7B-DT on macrophage M2 polarization and PDAC cell proliferation, migration, and invasion. In conclusion, KLHDC7B-DT enhanced malignant behaviors of PDAC cells via IL-6-induced macrophage M2 polarization and IL-6-activated STAT3 signaling in PDAC cells. The crosstalk between PDAC cells and macrophages induced by KLHDC7B-DT represents potential therapeutic target for PDAC.

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Section: Discussionmentioning

confidence: 99%

KLHDC7B-DT aggravates pancreatic ductal adenocarcinoma development via inducing cross-talk between cancer cells and macrophages

Wang

Yuan

et al. 2021

Clinical Science

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“…H 2 O 2 is widely used to induce apoptosis and ECM accumulation in HTM cells by mimicking oxidative stress 36‐38 . Herein, we found that H 2 O 2 treatment repressed HTM cell viability, promoted HTM cell apoptosis and increased ECM protein (collagen I, collagen III, fibronectin, MMP3, and MMP9) levels.…”

Section: Discussionmentioning

confidence: 81%

SNHG3 cooperates with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in human trabecular meshwork cells under oxidative stress

Yang

Zhou

et al. 2021

Environmental Toxicology

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Glaucoma is the main reason for irreversible blindness, and pathological increased intraocular pressure is the leading risk factor for glaucoma. It is reported that trabecular meshwork cell injury is closely associated with the elevated intraocular pressure. The current study aimed to investigate the role of small nucleolar RNA host gene 3 (SNHG3) in human trabecular meshwork (HTM) cells under oxidative stress. A series of experiments including real-time quantitative polymerase chain reaction, subcellular fractionation assay, western blot analysis, cell counting kit-8 assay, RNA pull down, flow cytometry analysis, and RNA immunoprecipitation assay were used to explore the biological function and regulatory mechanism of SNHG3 in HTM cells under oxidative stress. First, we observed that H 2 O 2 induced SNHG3 upregulation in HTM cells. Then, we found that SNHG3 silencing alleviated H 2 O 2 -induced oxidative damage in HTM cells. Moreover, snail family transcriptional repressor 2 (SNAI2) knockdown alleviated the oxidative damage induced by H 2 O 2 in HTM cells. Mechanistically, SNHG3 bound with ELAV like RNA binding protein 2 (ELAVL2) to stabilize SNAI2. Finally, SNAI2 overexpression counteracted the effect of SNHG3 silencing on H 2 O 2 -treated HTM cells. In conclusion, our results demonstrated that SNHG3 cooperated with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in HTM cells under oxidative stress.

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“…Haibo Li et al [21] provided evidence that lncRNA-MALAT1 could inhibit RGC apoptosis in glaucoma through activation of the PI3K/Akt signaling pathway. Shen W. et al [22] established that oxidative stress-induced lncRNA-RP11-820 plays a key role in regulating the miR-3178/MYOD1/ECM axis in HTMCs. Moreover, our previous work [23] had proved that knockdown of lncRNA NR_003923 in human Tenon's capsule fibroblast cells (HTFs) inhibited TGF-β-induced cell migration, proliferation, fibrosis, and autophagy and overexpression of IL22RA1 enhanced HTF migration and proliferation.…”

Section: Discussionmentioning

confidence: 99%

The potential role of long noncoding RNAs in primary open-angle glaucoma

Zhang

Zhao

Cao

et al. 2021

Graefes Arch Clin Exp Ophthalmol

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Purpose To identify the potential genes in human trabecular meshwork (TM) related to primary open-angle glaucoma (POAG). Methods First, long noncoding RNA (LncRNA) and mRNA expression profiles in TM samples from 4 control subjects and 4 POAG patients were accessed by microarray analyses. Then, twenty lncRNAs were validated by real-time quantitative PCR in the same samples from microarray analyses. Finally, eight highly expressed lncRNAs were further tested by real-time quantitative PCR in TM from 8 normal controls and 19 POAG patients. Expression data were normalized and analyzed using the R software. Pathway analyses were performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Results A total of 2179 lncRNAs and 923 mRNAs in the TM of POAG patients were significantly upregulated, and 3111 lncRNAs and 887 mRNAs were significantly downregulated. ENST00000552367, ENST00000582505, ENST00000609130, NR_029395, NR_038379, and ENST00000586949 expression levels were significantly higher in the TM from a different cohort of POAG patient than normal controls. Conclusion ENST00000552367, ENST00000582505, ENST000006091- 30, NR_029395, NR_038379, and ENST00000586949 may play essential roles in the development of POAG.

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Long non‐coding RNA RP11‐820 promotes extracellular matrix production via regulating miR‐3178/MYOD1 in human trabecular meshwork cells

Cited by 26 publications

References 43 publications

KLHDC7B-DT aggravates pancreatic ductal adenocarcinoma development via inducing cross-talk between cancer cells and macrophages

KLHDC7B-DT aggravates pancreatic ductal adenocarcinoma development via inducing cross-talk between cancer cells and macrophages

SNHG3 cooperates with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in human trabecular meshwork cells under oxidative stress

The potential role of long noncoding RNAs in primary open-angle glaucoma

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