Transcription Factor NFAT5 Promotes Glioblastoma Cell-driven Angiogenesis via SBF2-AS1/miR-338-3p-Mediated EGFL7 Expression Change

Yu, Hai; Zheng, Jian; Liu, Xiaobai; Xue, Yixue; Shen, Shuyuan; Zhao, Liye; Li, Zhen; Liu, Yunhui

doi:10.3389/fnmol.2017.00301

Cited by 60 publications

(46 citation statements)

References 53 publications

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“…Mechanistically, URRCC could crosstalk with EGFL7 via mediating histone H3 acetylation of EGFL7 promoter, which is consistent with the previously report [25, 43, 44]. In addition, EGFL7 was reported to active multiply signaling pathways in human tumors [43, 45–48]. In in vitro system, in vivo system and clinical specimen, we substantiated the upregulated URRCC was potent to promote EGFL7 expression, enhancing AKT pathway, and then contribute to tumorigenesis.…”

Section: Discussionsupporting

confidence: 90%

A positive feed-forward loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling promotes proliferation and metastasis of clear cell renal cell carcinoma

Zhai

Zhu

et al. 2019

Mol Cancer

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Background The aberrant expression of long noncoding RNAs (lncRNAs) has recently emerged as key molecules in human cancers; however, whether lncRNAs are implicated in the progression of clear cell renal cell carcinoma (ccRCC) remains unclear. Methods Candidate lncRNAs were selected using microarray analysis and quantitative real-time PCR (qRT-PCR) was performed to detect lncRNAs expression in human ccRCC tissues. Overexpression and knocking down experiments in vivo and in vitro were performed to uncover the biological roles of lncRNA-URRCC on ccRCC cell proliferation and invasion. Microarray, chromatin immunoprecipitation, Luciferase reporter assay and western blot were constructed to investigate the molecular mechanisms underlying the functions of lncRNA-URRCC. Results The microarray analysis and qRT-PCR identified a new lncRNA, URRCC, whose expression is upregulated in RCC samples and associated with poor prognosis, leading to promote ccRCC cell proliferation and invasion. Mechanistically, URRCC enhances the expression of EGFL7 via mediating histone H3 acetylation of EGFL7 promoter, activation of P-AKT signaling, and suppressing P-AKT downstream gene, FOXO3. In return, FOXO3 could inhibit the transcription of URRCC via binding to the special region on the promoter of URRCC. Conclusions Our data suggests that targeting this newly identified feed-back loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling may enhance the efficacy of existing therapy and potentially imparts a new avenue to develop more potent therapeutic approaches to suppress RCC progression. Electronic supplementary material The online version of this article (10.1186/s12943-019-0998-y) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 90%

A positive feed-forward loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling promotes proliferation and metastasis of clear cell renal cell carcinoma

Zhai

Zhu

et al. 2019

Mol Cancer

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“…According to the previous study, miR-338-3p had competitive relationship with the circSMO742 which transcripted by SMO, so we assumed that it might have targeting relationship with circSMO742 [25]. MiR-338-3p was reported to have correlation with tumor differentiation and down regulation of which could suppress terminal glial differentiation [26].…”

Section: Discussionmentioning

confidence: 89%

Circular RNA SMO sponges miR-338-3p to promote the growth of glioma by enhancing the expression of SMO

Zhang

Zhou

Wang

et al. 2019

Aging

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Glioma is one of the most common tumors in the brain and complete cure still a challenge. The present research aimed to investigate the molecular mechanism of circular RNA SMO (circSMO742) in glioma, via targeting miR-338-3p and regulating SMO expression. QRT-PCR was utilized to examine the expression profiles of circSMO742 and microRNA-338-3p (miR-338-3p) in glioma. SMO protein in glioma was tested via western blot. RNA pulldown assay and dual luciferase reporter assays were used to explore the targeting correlation between RNAs. MTT assay, transwell assays and flow cytometry were used to investigate cell proliferation, migration and invasion, and apoptosis, respectively. Tumor xenograft was done to ascertain the effect of circSMO742 knocking down on tumor growth. CircSMO742 and SMO were highly expressed in glioma tissues, while miR-338-3p expression was reduced. CircSMO742 together with SMO could promote cells proliferation, migration and invasion while inhibit cells apoptosis, whereas miR-338-3p showed negative impacts on the cell activity. Knocking down of circSMO742 suppressed glioma growing in vivo. CircSMO742 promoted glioma growth by sponging miR-338-3p to regulate SMO expression. Our research revealed a new molecular mechanism of glioma growth and provide a fresh perspective on circRNAs in glioma progression.

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“…Cell viability was performed using CCK-8 solution (Beyotime Biotechnology, Jiangsu, China) to assess the cell proliferation ability. The assay was performed as previously reported [27].…”

Section: Cell Viability Assaymentioning

confidence: 99%

Interaction of BACH2 with FUS promotes malignant progression of glioma cells via the TSLNC8–miR‐10b‐5p–WWC3 pathway

et al. 2020

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Glioma, a common malignant tumour of the human central nervous system, has poor prognosis and limited treatment options. Dissecting the biological mechanisms underlying glioma pathogenesis can facilitate the development of better therapies. Here, we investigated the endogenous expression of BTB and CNC homolog 2 (BACH2), fused in sarcoma (FUS), TSLNC8 and microRNA (miR)-10b-5p in glioma cells and tissues. We studied the interaction between BACH2 and FUS and its contribution to glioma progression. We demonstrated that the interaction between BACH2 and FUS promoted glioma progression via transcriptional inhibition of TSLNC8. Overexpression of TSLNC8 restrained glioma progression by suppressing miR-10b-5p. Binding of TSLNC8 to miR-10b-5p attenuated the suppression of WWC family member 3 (WWC3) by miR-10b-5p and activated the Hippo signalling pathway. Growth of subcutaneous xenografts could be inhibited by knockdown of BACH2 or FUS, by overexpressing TSLNC8 or a combination of the three, also leading to a prolonged survival in nude mice. Our results indicate that the BACH2 and FUS/TSLNC8/miR-10b-5p/WWC3 axis is responsible for glioma development and could serve as a potential target for the development of new glioma therapies.

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Transcription Factor NFAT5 Promotes Glioblastoma Cell-driven Angiogenesis via SBF2-AS1/miR-338-3p-Mediated EGFL7 Expression Change

Cited by 60 publications

References 53 publications

A positive feed-forward loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling promotes proliferation and metastasis of clear cell renal cell carcinoma

A positive feed-forward loop between LncRNA-URRCC and EGFL7/P-AKT/FOXO3 signaling promotes proliferation and metastasis of clear cell renal cell carcinoma

Circular RNA SMO sponges miR-338-3p to promote the growth of glioma by enhancing the expression of SMO

Interaction of BACH2 with FUS promotes malignant progression of glioma cells via the TSLNC8–miR‐10b‐5p–WWC3 pathway

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