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LncRNA NEAT1 Enhances Glioma Progression via Regulating the miR-128-3p/ITGA5 Axis

Chen, Jiakai, Wang, Handong, Wang, Junjun, Niu, Wenhao, Deng, Chulei, Zhou, Mengliang·2021·Molecular Neurobiology
DOI 10.1007/s12035-021-02474-yPMC PMC8497354
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Abstract

Accumulating evidences indicate that long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes the progression of glioma. In this study, we postulated that NEAT1 may act as a miR-128-3p sponge. Relative levels of NEAT1 and miR-128-3p expression in human glioma samples and GBM cells were detected using quantitative real-time PCR. By means of CCK-8 assays, transwell assays, and flow cytometric analysis, the biological functions of miR-128-3p and NEAT1 were investigated in U87MG and U251MG human GBM cell lines with stable miR-128-3p and NEAT1 knockdown or overexpression. The luciferase reports, RNA pull-down assay, and RNA immunoprecipitation assay were conducted to determine the relevance of NEAT1 and miR-128-3p in glioma. As a result, high expression of NEAT1 and lack of miR-128-3p were observed in glioma specimens and cells. By binding to anti-oncogene miR-128-3p in the nucleus, NEAT1 enhanced tumorigenesis and glioma development. Further experiments suggested that ITGA5 expression was increased in glioma tissues and was found to be connected with miR-128-3p. Additionally, NEAT1 facilitated ITGA5 expression via competitively binding to miR-128-3p. For this reason, ITGA5 would not be decomposed by miR-128-3p and could activate FAK signaling pathway, thereby promoting cell growth. Collectively, these results indicated that the NEAT1/miR-128-3p/ITGA5 axis was involved in glioma initiation and progression, and might offer a potential novel strategy for treatment of glioma.

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Fig. 1 In glioma tissues and GBM cell lines, NEAT1 was upregulated whereas miR-128-3p showed an obvious decrease, and miR-128-3p was localized in both the nucleus and cytoplasm. a, b qRT-PCR showing NEAT1 and miR-128-3p expression levels in normal brain tissues (NBT) and different grades of glioma tissues (LGG, HGG), each group had 10 samples. *p < 0.05, **p < 0.01, ***p < 0.001. c, d Expression of NEAT1 and miR-128-3p in normal human astrocytes (HA) and GBM cell lines (U87MG, U118MG, A172, U251MG). *p < 0.05, **p < 0.01, ***p < 0.001 VS HA. e FISH assay verified the subcellular localization of miR-128-3p
Fig. 1 In glioma tissues and GBM cell lines, NEAT1 was upregulated whereas miR-128-3p showed an obvious decrease, and miR-128-3p was localized in both the nucleus and cytoplasm. a, b qRT-PCR showing NEAT1 and miR-128-3p expression levels in normal brain tissues (NBT) and different grades of glioma tissues (LGG, HGG), each group had 10 samples. *p < 0.05, **p < 0.01, ***p < 0.001. c, d Expression of NEAT1 and miR-128-3p in normal human astrocytes (HA) and GBM cell lines (U87MG, U118MG, A172, U251MG). *p < 0.05, **p < 0.01, ***p < 0.001 VS HA. e FISH assay verified the subcellular localization of miR-128-3pCC BY · PubMed Central
Fig. 2 NEAT1 was a direct target gene of miR-128-3p. a Linear regression analysis between expression levels of NEAT1 and miR-128-3p in glioma tissues. b–e Effects of lentiviral transfections were confirmed by qRT-PCR. An inversely relationship was observed between expression levels of NEAT1 and miR-128-3p in glioma cells. *p < 0.05, ***p < 0.001 VS shCtrl group; #p < 0.05, ##p < 0.01, ###p < 0.001 VS pLV-Ctrl group. f The hypothesized wild-type or mutational miR-128-3p binding sites in ITGA5. g Luciferase activities in U87MG cells co-transfected with vector NEAT1-3′UTR-WT or NEAT1-3′UTR-MUT and miR-128-3p mimics or NC mimics was analyzed by Luciferase reporter assay. ***p < 0.001. h Specific association between NEAT1 and miR-128-3p following a RNA pull-down assay in U87MG cells. ***p < 0.001. i, j RIP assay indicating both of NEAT1 and miR-128-3p were enriched by anti-AGO2 in U87MG cells, whether miR-128-3p was overexpressed beforehand or not. *p < 0.05, ***p < 0.001 VS anti-IgG group
Fig. 2 NEAT1 was a direct target gene of miR-128-3p. a Linear regression analysis between expression levels of NEAT1 and miR-128-3p in glioma tissues. b–e Effects of lentiviral transfections were confirmed by qRT-PCR. An inversely relationship was observed between expression levels of NEAT1 and miR-128-3p in glioma cells. *p < 0.05, ***p < 0.001 VS shCtrl group; #p < 0.05, ##p < 0.01, ###p < 0.001 VS pLV-Ctrl group. f The hypothesized wild-type or mutational miR-128-3p binding sites in ITGA5. g Luciferase activities in U87MG cells co-transfected with vector NEAT1-3′UTR-WT or NEAT1-3′UTR-MUT and miR-128-3p mimics or NC mimics was analyzed by Luciferase reporter assay. ***p < 0.001. h Specific association between NEAT1 and miR-128-3p following a RNA pull-down assay in U87MG cells. ***p < 0.001. i, j RIP assay indicating both of NEAT1 and miR-128-3p were enriched by anti-AGO2 in U87MG cells, whether miR-128-3p was overexpressed beforehand or not. *p < 0.05, ***p < 0.001 VS anti-IgG groupCC BY · PubMed Central
Fig. 3 NEAT1/miR-128-3p axis participated in glioma progression in vitro. a CCK-8 assays were carried out to appraise the effects of NEAT1 and miR-128-3p on cell viability in U87MG and U251MG cells. b Transwell assays were applied to measure the effects of NEAT1 and miR-128-3p on cell viability in U87MG and U251MG cells. c, d Flow cytometry were employed to evaluate the effects of NEAT1 and miR-128-3p on cell apoptosis and cell cycle in U87MG and U251MG cells. **p < 0.01, ***p < 0.001 VS shCtrl group; #p < 0.05, ##p < 0.01, ###p < 0.001 VS anti-miR-128-3p group
Fig. 3 NEAT1/miR-128-3p axis participated in glioma progression in vitro. a CCK-8 assays were carried out to appraise the effects of NEAT1 and miR-128-3p on cell viability in U87MG and U251MG cells. b Transwell assays were applied to measure the effects of NEAT1 and miR-128-3p on cell viability in U87MG and U251MG cells. c, d Flow cytometry were employed to evaluate the effects of NEAT1 and miR-128-3p on cell apoptosis and cell cycle in U87MG and U251MG cells. **p < 0.01, ***p < 0.001 VS shCtrl group; #p < 0.05, ##p < 0.01, ###p < 0.001 VS anti-miR-128-3p groupCC BY · PubMed Central
Fig. 4 NEAT1/miR-128-3p axis was involved in glioma growth in vivo. a Subcutaneous xenotransplanted GBM model was established by intratumorally injecting U87MG cells into the right flank of nude mice. Tumors were harvested 28 days after injection, and tumor volume curves of nude mice in each group (n = 5) were plotted. ***p < 0.001 VS shCtrl group; ###p < 0.001 VS anti-miR-128-3p group. b IF staining of Ki-67 and TUNEL staining of tumor sections collected from nude mice were performed. Scale bar represents 50 mm
Fig. 4 NEAT1/miR-128-3p axis was involved in glioma growth in vivo. a Subcutaneous xenotransplanted GBM model was established by intratumorally injecting U87MG cells into the right flank of nude mice. Tumors were harvested 28 days after injection, and tumor volume curves of nude mice in each group (n = 5) were plotted. ***p < 0.001 VS shCtrl group; ###p < 0.001 VS anti-miR-128-3p group. b IF staining of Ki-67 and TUNEL staining of tumor sections collected from nude mice were performed. Scale bar represents 50 mmCC BY · PubMed Central
Fig. 5 ITAG5 was an oncogene of glioma regulated by the NEAT1/miR-128-3p axis. a Profile of ITGA5 expression in glioma specimens following qRT-PCR. b Linear regression showing the relationship between expression levels of ITGA5 and miR-128-3p in glioma samples. c–g ITGA5 expression was assessed by qRT-PCR and western blot analysis in U87MG and U251MG cells transfected with various lentivirus about NEAT1 and miR-128-3p to explore the part of ITGA5 in them. *p < 0.05, **p < 0.01 VS shCtrl group; #p < 0.05, ##p < 0.01, ###p < 0.001 VS pLV-Ctrl group; & p < 0.05 VS anti-miR-128-3p group
Fig. 5 ITAG5 was an oncogene of glioma regulated by the NEAT1/miR-128-3p axis. a Profile of ITGA5 expression in glioma specimens following qRT-PCR. b Linear regression showing the relationship between expression levels of ITGA5 and miR-128-3p in glioma samples. c–g ITGA5 expression was assessed by qRT-PCR and western blot analysis in U87MG and U251MG cells transfected with various lentivirus about NEAT1 and miR-128-3p to explore the part of ITGA5 in them. *p < 0.05, **p < 0.01 VS shCtrl group; #p < 0.05, ##p < 0.01, ###p < 0.001 VS pLV-Ctrl group; & p < 0.05 VS anti-miR-128-3p groupCC BY · PubMed Central
Fig. 6 miR-128-3p mediated the pro-oncogenic effects of ITGA5. a The predicted wild-type or mutated miR-128-3p binding sites in ITGA5. b Luciferase activities in U87MG cells co-transfected with vector ITGA5-3′UTR-WT or ITGA5-3′UTR-MUT and miR-128-3p mimics or NC mimics as determined with luciferase reporter assay. ***p < 0.001. c The effects of NEAT1 and miR-128-3p on the proliferation of U87MG and U251MG cells as examined with CCK-8 assays. d The effects of NEAT1 and miR-128-3p on the migration and invasion of U87MG and U251MG cells as evaluated with transwell assays. e, f The effects of NEAT1 and miR-128-3p on apoptosis and cell cycle progression of U87MG and U251MG cells were determined by flow cytometry assays. *p < 0.05, **p < 0.01, ***p < 0.001 VS pLV-Ctrl group; #p < 0.05, ##p < 0.01, ###p < 0.001 VS pre-miR-128-3p group
Fig. 6 miR-128-3p mediated the pro-oncogenic effects of ITGA5. a The predicted wild-type or mutated miR-128-3p binding sites in ITGA5. b Luciferase activities in U87MG cells co-transfected with vector ITGA5-3′UTR-WT or ITGA5-3′UTR-MUT and miR-128-3p mimics or NC mimics as determined with luciferase reporter assay. ***p < 0.001. c The effects of NEAT1 and miR-128-3p on the proliferation of U87MG and U251MG cells as examined with CCK-8 assays. d The effects of NEAT1 and miR-128-3p on the migration and invasion of U87MG and U251MG cells as evaluated with transwell assays. e, f The effects of NEAT1 and miR-128-3p on apoptosis and cell cycle progression of U87MG and U251MG cells were determined by flow cytometry assays. *p < 0.05, **p < 0.01, ***p < 0.001 VS pLV-Ctrl group; #p < 0.05, ##p < 0.01, ###p < 0.001 VS pre-miR-128-3p groupCC BY · PubMed Central
Fig. 7 ITGA5 activated FAK signaling pathway in glioma cells. a Expression levels of the FAK signaling pathway related proteins such as phosphorylated and non-phosphorylated forms of FAK, total and cleaved caspase-3 as well as cyclin D1 were quantified by western blotting assays. *p < 0.05, **p < 0.01 VS pLV-Ctrl group; #p < 0.05, ##p < 0.01 VS pre-miR-128-3p group
Fig. 7 ITGA5 activated FAK signaling pathway in glioma cells. a Expression levels of the FAK signaling pathway related proteins such as phosphorylated and non-phosphorylated forms of FAK, total and cleaved caspase-3 as well as cyclin D1 were quantified by western blotting assays. *p < 0.05, **p < 0.01 VS pLV-Ctrl group; #p < 0.05, ##p < 0.01 VS pre-miR-128-3p groupCC BY · PubMed Central

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Metadata

Authors
Chen, J., Wang, H., Wang, J., Niu, W., Deng, C., & Zhou, M.
ORCID
Venue
Molecular Neurobiology
Publisher
Springer Science and Business Media LLC
Published
2021-07-15
Volume
58
Issue
10
Pages
5163-5177
ISSN
  • 0893-7648
  • 1559-1182
DOI
10.1007/s12035-021-02474-y
PMC
PMC8497354
Cited by
26
References
0
Language
en
Licence
Funders
National Natural Science Foundation of China (No.81672503 and No.81702484)

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