KLF5-Modulated lncRNA NEAT1 Contributes to Tumorigenesis by Acting as a Scaffold for BRG1 to Silence GADD45A in Gastric Cancer

Ma, Pei; Pan, Yongsheng; Yang, Fan; Fang, Yuan; Liu, Weitao; Zhao, Cheng; Tao, Yu; Xie, Mengyan; Jing, Xingming; Wu, Xi; Sun, Chongqi; Li, Wei; Xu, Tongpeng; Shu, Yongqian

doi:10.1016/j.omtn.2020.09.003

Cited by 24 publications

(22 citation statements)

References 44 publications

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“…In line with our data, KLF5 was also discovered as a transcription factor to facilitate lncRNAs expression in other malignancies. For instance, KLF5-activated lncRNA NEAT1 accelerated gastric cancer progression via serving as a scaffold for BRG1 to down-regulate GADD45A expression [ 34 ]. KLF5-regulated lncRNA RP1 contributed to cell proliferation and metastasis in breast cancer through suppressing p27kip1 translation [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway

Shi

Yang

et al. 2021

J Exp Clin Cancer Res

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Background Non-small cell lung cancer (NSCLC) is a major histological subtype of lung cancer with high mortality and morbidity. A substantial amount of evidence demonstrates long non-coding RNAs (lncRNA) as critical regulators in tumorigeneis and malignant progression of human cancers. The oncogenic role of BBOX1 anti-sense RNA 1 (BBOX1-AS1) has been reported in several tumors. As yet, the potential functions and mechanisms of BBOX1-AS1 in NSCLC are obscure. Methods The gene and protein expression was detected by qRT-PCR and western blot. Cell function was determined by CCK-8, colony forming, would healing and transwell assays. Bioinformatics tools, ChIP assays, dual luciferase reporters system and RNA pull-down experiments were used to examine the interaction between molecules. Subcutaneous tumor models in nude mice were established to investigate in vivo NSCLC cell behavior. Results BBOX1-AS1 was highly expressed in NSCLC tissues and cells. High BBOX1-AS1 expression was associated with worse clinical parameters and poor prognosis. BBOX1-AS1 up-regulation was induced by transcription factor KLF5. BBOX1-AS1 deficiency resulted in an inhibition of cell proliferation, migration, invasion and EMT in vitro. Also, knockdown of BBOX1-AS1 suppressed NSCLC xenograft tumor growth in mice in vivo. Mechanistically, BBOX1-AS1 acted act as a competetive “sponge” of miR-27a-5p to promote maternal embryonic leucine zipper kinase (MELK) expression and activate FAK signaling. miR-27a-5p was confirmed as a tumor suppressor in NSCLC. Moreover, BBOX1-AS1-induced increase of cell proliferation, migration, invasion and EMT was greatly reversed due to the overexpression of miR-27a-5p. In addition, the suppressive effect of NSCLC progression owing to BBOX1-AS1 depletion was abated by the up-regulation of MELK. Consistently, BBOX1-AS1-mediated carcinogenicity was attenuated in NSCLC after treatment with a specific MELK inhibitor OTSSP167. Conclusions KLF5-induced BBOX1-AS1 exerts tumor-promotive roles in NSCLC via sponging miR-27a-5p to activate MELK/FAK signaling, providing the possibility of employing BBOX1-AS1 as a therapeutic target for NSCLC patients.

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Section: Discussionmentioning

confidence: 99%

KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway

Shi

Yang

et al. 2021

J Exp Clin Cancer Res

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“…LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) is an essential component of the nuclear paraspeckle substructure [9]. Particularly, NEAT1 is a pro-oncogenic factor that plays a positive role in various solid tumors, such as liver, prostate, and gastric cancers, as well as renal cell carcinomas and glioma [10][11][12][13][14]. In glioma, NEAT1 has been found to regulate tumor progression via mTOR signaling pathway [15].…”

Section: Introductionmentioning

confidence: 99%

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

Chen

Wang

et al. 2021

Mol Neurobiol

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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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“…Of tens of thousands of metazoan lncRNAs discovered from cDNA libraries and RNAseq data by high throughput transcriptome projects, only a handful of lncRNAs have been functionally characterized. The investigations on this small cohort of lncRNAs have demonstrated that these noncoding transcripts can serve as scaffolds or guides to regulate protein-protein or protein-DNA interactions [28][29][30][31] or can modulate post-translational modification of nonhistone proteins [32]. Moreover, lncRNAs are capable of controlling microRNAs (miRNAs) [33][34][35], and function as enhancers to influence gene transcription, when transcribed from the enhancer regions (enhancer RNA) [36][37][38] or their neighboring loci (noncoding RNA activator) [39,40].…”

Section: Long Non-coding Rna Structures and Functionsmentioning

confidence: 99%

Circulating Long Non-Coding RNAs as Novel Potential Biomarkers for Osteogenic Sarcoma

Moonmuang

Chaiyawat

Jantrapirom

et al. 2021

Cancers

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Circulating cell-free nucleic acids recently became attractive targets to develop non-invasive diagnostic tools for cancer detection. Along with DNA and mRNAs, transcripts lacking coding potential (non-coding RNAs, ncRNAs) directly involved in the process of tumor pathogenesis have been recently detected in liquid biopsies. Interestingly, circulating ncRNAs exhibit specific expression patterns associated with cancer and suggest their role as novel biomarkers. However, the potential of circulating long ncRNAs (c-lncRNAs) to be markers in osteosarcoma (OS) is still elusive. In this study we performed a systematic review to identify thirteen c-lncRNAs whose altered expression in blood associate with OS. We herein discuss the potential impact that these c-lncRNAs may have on clinical decision-making in the management of OS. Overall, we aimed to provide novel insights that can contribute to the development of future precision medicine in oncology.

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KLF5-Modulated lncRNA NEAT1 Contributes to Tumorigenesis by Acting as a Scaffold for BRG1 to Silence GADD45A in Gastric Cancer

Cited by 24 publications

References 44 publications

KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway

KLF5-induced BBOX1-AS1 contributes to cell malignant phenotypes in non-small cell lung cancer via sponging miR-27a-5p to up-regulate MELK and activate FAK signaling pathway

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

Circulating Long Non-Coding RNAs as Novel Potential Biomarkers for Osteogenic Sarcoma

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