Knockdown of long non-coding RNA LINC00467 inhibits glioma cell progression via modulation of E2F3 targeted by miR-200a

Gao, Shuzi; Duan, Haixia; An, Dezhu; Yi, Xinfeng; Li, Jiayan; Liao, Changchun

doi:10.1080/15384101.2020.1792127

Cited by 10 publications

(8 citation statements)

References 48 publications

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“…LINC00467 expression is aberrantly upregulated in multiple tumor tissues and can enhance cell proliferation in neuroblastoma ( 15 ), lung cancer ( 16 ), and glioma cells ( 17 ). LINC00467 expression is closely associated with worse prognosis of these tumors.…”

Section: Discussionmentioning

confidence: 99%

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

et al. 2021

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BackgroundThe long non-coding RNA LINC00467 plays a vital role in many malignancies. Nevertheless, the role of LINC00467 in prostate carcinoma (PC) is unknown. Herein, we aimed to explore the mechanism by which LINC00467 regulates PC progression.MethodsWe used bioinformatics analyses and RT-qPCR to investigate the expression of LINC00467 in PC tissues and cells. The function of LINC00467 in the progression of PC was confirmed by loss-of-function experiments. PC cell proliferation was assessed by CCK-8 and EdU assays. The cell cycle progression of PC cells was examined by flow cytometry. Moreover, Transwell assays were used to investigate the migration and invasion of PC cells. Western blot assays were used to detect the expression of factors associated with epithelial–mesenchymal transition. The interactions of LINC00467 with prostate cancer progression and M2 macrophage polarization were confirmed by RT-qPCR. The subcellular localization of LINC00467 was investigated via the fractionation of nuclear and cytoplasmic RNA. Bioinformatics data analysis was used to predict the correlation of LINC00467 expression with miR-494-3p expression. LINC00467/miR-494-3p/STAT3 interactions were identified by using a dual-luciferase reporter system. Finally, the influence of LINC00467 expression on PC progression was investigated with an in vivo nude mouse model of tumorigenesis.ResultsWe established that LINC00467 expression was upregulated in PC tissues and cells. Downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion. Downregulated LINC00467 expression similarly inhibited PC cell migration via M2 macrophage polarization. Western blot analysis showed that LINC00467 could regulate the STAT3 pathway. We established that LINC00467 is mainly localized to the cytoplasm. Bioinformatics analysis and rescue experiments indicated that LINC00467 promotes PC progression via the miR-494-3p/STAT3 axis. Downregulated LINC00467 expression was also able to suppress PC tumor growth in vivo.ConclusionsOur study reveals that LINC00467 promotes prostate cancer progression via M2 macrophage polarization and the miR-494-3p/STAT3 axis.

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Section: Discussionmentioning

confidence: 99%

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

et al. 2021

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“…Several initiated signaling pathways, including linc00467/miR-20b-5p/cyclin D1 pathway [ 20 ] and STAT1-induced upregulation of linc00467 promoted lung adenocarcinoma progression through epigenetically suppressing dickkopf WNT signaling pathway inhibitor 1 to activate Wnt/β-catenin signaling [ 16 ]. Regarding glioma, studies have demonstrated that linc00467/DNA methyltransferase 1/p53 pathway, and linc00467/miR-200a/E2F transcription factor 3 pathway might be involved in the occurrence of glioma [ 21 , 30 ]. In this study, we have further discovered that linc00467 was significantly upregulated in GC cell lines compared with control GES-1.…”

Section: Discussionmentioning

confidence: 99%

Linc00467 promotion of gastric cancer development by directly regulating miR-7-5p expression and downstream epidermal growth factor receptor

et al. 2021

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Linc00467 is a vital regulator in tumor progression. This study explores the molecular mechanisms of linc00467 in gastric cancer (GC). Linc00467 expression was obtained and analyzed in GC tissue through exploration in the cancer genome atlas database. Then, real-time quantitative polymerase chain reaction was used to detect linc000467 expression in GC cells. Cell functions were observed using cell counting Kit-8, Transwell assay, Western blotting to testify the proliferation, migration, invasion, and the relative expression of epidermal growth factor receptor (EGFR) in GC cells. Moreover, a dual-luciferase reporter gene assay was used to verify the relationship between linc00467 and miR-7-5p. Results showed that the expression of linc00467 was overexpressed in GC. Linc00467 silencing decreased the GC cell proliferation, migration, and invasion. With mRNA verification and combined previous research, linc00467 directly regulated the miR-7-5p expression and downstream EGFR expression. Inhibited miR-7-5p could restore cell function, EGFR expression of GC cells when linc00467 knockdown occurs. Altogether, linc00467 directly regulates the miR-7-5p and EGFR signaling pathway to promote GC proliferation, migration, and invasion.

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“…Moreover, concordant with our results, silence of LINC00467 has been demonstrated to curb malignant properties of GC cells by targeting microRNA-7-5p [ 9 ]. Of note, LINC00467 knockdown diminished glioma U87 and U251 cell malignant properties [ 35 , 36 ]. In addition, ectopically expressed LINC00467 contributed to elevation of cell malignant properties in osteosarcoma [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Downregulated Reprimo by LINC00467 participates in the growth and metastasis of gastric cancer

2022

Bioengineered

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Gastric cancer (GC) as an aggressive malignancy still causes a global health problem. It has been documented that long noncoding RNAs are involved in GC development. Therefore, this research was designed to explore the role of LINC00467 in the growth and metastasis of GC. The expression of LINC00467 and Reprimo in GC tissues and cells was detected. The binding relationship among LINC00467, DNA methyltransferase 1 (DNMT1) and Reprimo was assessed following. Reprimo promoter methylation was detected by methylation sequencing. GC cell lines overexpressing or knock downing LINC00467 were constructed for pinpointing the effect of LINC00467 on cell functions as well as growth and metastasis of GC cells in vivo . LINC00467 was highly expressed, whereas Reprimo was poorly expressed in GC tissues and cells. Mechanically, LINC00467 promoted the methylation and decreased the expression of Reprimo promoter by recruiting DNMT1 in GC cells. Knockdown of LINC00467 diminished the malignant properties of GC cells. Knockdown of LINC00467 reduced tumorigenesis and metastasis of GC cells in vivo . LINC00467 might exert oncogenic effects in GC via Reprimo downregulation by recruiting DNMT1.

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Knockdown of long non-coding RNA LINC00467 inhibits glioma cell progression via modulation of E2F3 targeted by miR-200a

Cited by 10 publications

References 48 publications

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis

Linc00467 promotion of gastric cancer development by directly regulating miR-7-5p expression and downstream epidermal growth factor receptor

Downregulated Reprimo by LINC00467 participates in the growth and metastasis of gastric cancer

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