Long non-coding RNA HOXB-AS1 promotes proliferation, migration and invasion of glioblastoma cells via HOXB-AS1/miR-885-3p/HOXB2 axis

Chen, X; Li, L Q; Qiu, Xiaofei; Wu, Hao

doi:10.4149/neo_2018_180606n377

Cited by 37 publications

(31 citation statements)

References 28 publications

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“…15 Moreover, miR-885-3p acted as a tumor suppressor in glioblastoma and gastric cancer. 16,17 Our studies showed that miR-885-3p was down-regulated in PBMCs from T1D patients, which was consistent with recent findings from Zuraek et al. 10 Consistently, our results indicated that miR-885-3p had inhibitory actions on the immune response of THP-1 cells.…”

Section: Discussionsupporting

confidence: 92%

“…12 MiR-885-3p could target γ-synuclein 3'-UTR and repress γ-synuclein, which may be involved in the tumor metastasis. 16,17 Our studies showed that miR-885-3p was down-regulated in PBMCs from T1D patients, which was consistent with recent findings from Zuraek et al. 14 MiR-885-3p could target the 3'-UTR of vitamin D receptor and contributed to the development of pressure ulcers.…”

Section: Tlr4 Was Directly Targeted By Mir-885-3psupporting

confidence: 91%

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MiR‐885‐3p is down‐regulated in peripheral blood mononuclear cells from T1D patients and regulates the inflammatory response via targeting TLR4/NF‐κB signaling

Zhang

Wang

et al. 2019

The Journal of Gene Medicine

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Background: Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the progressive destruction of insulin-production pancreatic β cells. Recently, microRNAs (miRNAs) have emerged as important regulators in T1D. The present study aimed to determine miR-885-3p expression in T1D patients and to examine the effects of miR-885-3p on the inflammatory response in human monocytes.Methods: Relevant gene expression levels were determined by a quantitative polymerase chain reaction; western blotting and enzyme-linked immunosorbent assays determined the respective protein levels; and the interaction between miRNA and the downstream targets was evaluated using a luciferase reporter assay.Results: MiR-885-3p is down-regulated and the levels of pro-inflammatory cytokines are increased in peripheral blood mononuclear cells (PBMCs) from T1D patients compared to healthy controls. MiR-885-3p overexpression suppressed mRNA expression and secreted protein levels of pro-inflammatory cytokines in THP-1. A luciferase reporter assay showed that miR-885-3p directly targeted the 3'untranslated region of Toll-like receptor 4 (TLR4) and miR-885-3p overexpression down-regulated TLR4 expression in THP-1 cells. The TLR4 mRNA expression level was increased in PBMCs isolated from T1D patients compared to heathy controls.TLR4 overexpression increased the secretion of pro-inflammatory cytokines and enhanced the activity of NF-κB signaling, and also attenuated the inhibitory effects of miR-885-3p overexpression on pro-inflammatory cytokine secretion and the activity of NF-κB signaling in THP-1 cells. Conclusions:The present study identified the down-regulation of miR-885-3p and up-regulation of TLR4 in PBMCs isolated from T1D patients. Further mechanistic data demonstrated that miR-885-3p overexpression represses the production of proinflammatory cytokines via targeting TLR4/NF-κB signaling in THP-1 cells.

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Section: Discussionsupporting

confidence: 92%

Section: Tlr4 Was Directly Targeted By Mir-885-3psupporting

confidence: 91%

MiR‐885‐3p is down‐regulated in peripheral blood mononuclear cells from T1D patients and regulates the inflammatory response via targeting TLR4/NF‐κB signaling

Zhang

Wang

et al. 2019

The Journal of Gene Medicine

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“…24,25 Moreover, lncRNA HOXB-AS1 promoted proliferation, migration and invasion of glioblastoma cells via miR-885-3p/HOXB2 axis. 16 It has also been reported that lncRNA RGMB-AS1 promoted glioma growth and invasion through miR-1200/HOXB2 axis. 26 In the present study, LINC00662 also facilitated ESCC progression by regulating miR-340-5p/HOXB2 axis.…”

Section: Discussionmentioning

confidence: 97%

“…13,14 In addition, miR-4324 has been found to function as a tumor suppressor in colorectal cancer by targeting HOXB2, 15 and lncRNA HOXB-AS1 promoted proliferation, migration and invasion of glioblastoma cells via miR-885-3p/HOXB2 axis. 16 Moreover, HOXB2 has been demonstrated to be a target of miR-340 in acute myeloid leukemia. 17 However, the role of HOXB2 in ESCC has not been reported in previous studies.…”

Section: Introductionmentioning

confidence: 99%

LINC00662 promotes cell viability and metastasis in esophageal squamous cell carcinoma by sponging miR‐340‐5p and upregulating HOXB2

et al. 2020

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Background: Previous studies have shown that lncRNA LINC00662 plays an important role in pathogenesis of malignancies. The purpose of this study was to elucidate the regulatory mechanism of LINC00662 in esophageal squamous cell carcinoma (ESCC). Methods: In this study, the regulatory mechanism of LINC00662 was investigated by RT-qPCR. MTT, transwell and dual luciferase reporter assays. Results: Upregulation of LINC00662 was found in ESCC and associated with worse clinical outcomes in ESCC patients. More importantly, knockdown of LINC00662 restrained cell proliferation, migration and invasion in ESCC. In addition, LINC00662 acts as a molecular sponge for miR-340-5p in ESCC, and miR-340-5p directly targets HOXB2. HOXB2 expression can be positively regulated by LINC00662 in ESCC. Furthermore, HOXB2 downregulation or miR-340-5p overexpression weakened the carcinogenesis of LINC00662 in ESCC. Conclusions: LncRNA LINC00662 promotes the progression of ESCC by upregulating HOXB2 by sponging miR-340-5p.

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“…It was latterly found that HOXB‐AS1 played a tumor‐promoting role in GBM (Chen et al, 2019). The present study purposed to inspect more sophisticated mechanism underlying HOXB‐AS1 in GBM.…”

Section: Discussionmentioning

confidence: 99%

HOXB‐AS1 accelerates the tumorigenesis of glioblastoma via modulation of HOBX2 and HOBX3 at transcriptional and posttranscriptional levels

Mao

et al. 2020

Journal Cellular Physiology

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Glioblastoma (GBM) is the most universal and invasive brain tumor among adults. Increasing studies have reported that long noncoding RNAs play vital roles in regulating downstream molecules at the transcriptional or posttranscriptional level in tumor progression. The purpose of the current research was to inquire the modulation mechanism by which homeobox B cluster antisense RNA 1 (HOXB-AS1) functioned in GBM. Our study first discovered the lifted expression of HOXB-AS1 and its nearby genes HOXB2 and HOXB3 in GBM and the positive relationship between HOXB-AS1 and HOXB2 or HOXB3. Loss-of-function assays and in vivo study detected that silencing of HOXB-AS1, HOXB2, or HOXB3 restrained the proliferation and induced the apoptosis in GBM. In addition, mechanism experiments demonstrated that HOXB-AS1 recruited interleukin enhancer-binding factor 3 (ILF3) to regulate HOXB2 and HOXB3 expression at the transcriptional level, and HOXB-AS1 sponged miR-186-5p to modulate HOXB2 and HOXB3 expression at posttranscriptional level. Finally, the regulatory mechanism of HOXB-AS1 in GBM was certified through rescue experiments. Our results indicated that HOXB-AS1 boost the HOXB2 or HOXB3 expression at the transcriptional and posttranscriptional levels. We detected the HOXB-AS1-ILF3-HOXB2/HOXB3 axis and HOXB-AS1-miR-186-5p-HOXB2/HOXB3 axis driving the GBM progression, which might generate more effective diagnostic biomarkers and therapeutic targets for patients with GBM.

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Long non-coding RNA HOXB-AS1 promotes proliferation, migration and invasion of glioblastoma cells via HOXB-AS1/miR-885-3p/HOXB2 axis

Cited by 37 publications

References 28 publications

MiR‐885‐3p is down‐regulated in peripheral blood mononuclear cells from T1D patients and regulates the inflammatory response via targeting TLR4/NF‐κB signaling

MiR‐885‐3p is down‐regulated in peripheral blood mononuclear cells from T1D patients and regulates the inflammatory response via targeting TLR4/NF‐κB signaling

LINC00662 promotes cell viability and metastasis in esophageal squamous cell carcinoma by sponging miR‐340‐5p and upregulating HOXB2

HOXB‐AS1 accelerates the tumorigenesis of glioblastoma via modulation of HOBX2 and HOBX3 at transcriptional and posttranscriptional levels

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