BCLAF1 promotes cell proliferation, invasion and drug-resistance though targeting lncRNA NEAT1 in hepatocellular carcinoma

Mou, Shaojiao; Yang, Pengfei; Yi-pin, Liu; Xu, Ning; Jiang, Weiwei; Yue, Wenjing

doi:10.1016/j.lfs.2019.117177

Cited by 39 publications

(30 citation statements)

References 26 publications

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“…Understanding the mechanisms of resistance in CRC is imperative to improve the survival. In recent years, studies have shown that NEAT1 was associated with resistance to chemotherapy in hepatocellular carcinoma 24 , endometrial cancer 25 and others. Moreover, the effects of NEAT1 and cancer stem cells in breast cancer have also been reported 17 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 remodels chromatin to promote the 5-Fu resistance by maintaining colorectal cancer stemness

Zhu

Yuan

et al. 2020

Cell Death Dis

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Resistance of chemotherapy is one of causes of recurrence and poor prognosis in patients with colorectal cancer (CRC). The role of differentially expressed long non-coding RNA (lncRNA) in 5-fluorouracil (5-Fu) resistance has not been fully elucidated. Here we observed that lncRNA NEAT1 was associated with 5-Fu resistance in CRC. Our Functional studies showed that NEAT1 promoted 5-Fu resistance in colorectal cells. In addition, A-TAC sequencing and chromatin immunoprecipitation (ChIP) showed that NEAT1 affected chromatin remodeling, increased the acetylation levels of histones, increased their enrichment at the promoters of ALDH1 and c-Myc, and promoted the expression of ALDH1 and c-Myc. Taken together, our study suggested that NEAT1 promoted 5-Fu resistance and cancer stemness by remodeling chromatin. Our finding provides a novel role of NEAT1 and may provide a new strategy for the treatment of CRC 5-Fu resistance.

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Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 remodels chromatin to promote the 5-Fu resistance by maintaining colorectal cancer stemness

Zhu

Yuan

et al. 2020

Cell Death Dis

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“…Subsequently, we demonstrated that ATF2 promoted NEAT1 transcription via binding to the NEAT1 promoter in LUAD cells. In hepatocellular carcinoma, BCLAF1 promotes cell proliferation, invasion and 5-Fluorouracil resistance though targeting NEAT1 [31]. In lung cancer cells, NEAT1 and MALAT1 have been proved to be downstream effectors of Oct4-induced lung cancer proliferation, migration and invasion [21].…”

Section: Discussionmentioning

confidence: 99%

The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression

Liu

Wang

et al. 2020

Cancer Cell Int

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Background Activating transcription factor 2 (ATF2), a member of the activator protein 1 (AP-1) transcription factor family, has been shown to be involved in the pathobiology of numerous cancers. However, the biological role and mechanism of ATF2 in lung adenocarcinoma (LUAD) remains to be elucidated. Methods The expression of ATF2, NEAT1 and miR-26a-5p in LUAD tissues and cell lines was detected by qRT-PCR and western blotting. The interaction between ATF2, NEAT1, and miR-26a-5p was validated by chromatin immunoprecipitation, luciferase reporter assay and RNA immunoprecipitation. Cell proliferation, invasion and tumorigenesis of LUAD cells were analyzed by using CCK8, transwell invasion assay and xenograft tumor model. Results We confirmed that ATF2 expression was increased in LUAD tissues compared with normal adjacent lung tissues. Functional experiments showed that ATF2 positively regulated cell proliferation and invasion in LUAD cells. Moreover, we identified that NEAT1 expression was increased in LUAD tissues and positively correlated with ATF2 expression. Mechanistically, ATF2 could bind to the promoter of NEAT1 to promote its transcription. Rescue experiments showed that ATF2 exerted its oncogenic function in LUAD, at least, partly through NEAT1 upregulation. In turn, NEAT1 could positively regulate ATF2 expression and form a positive feedback loop in LUAD cells. Furthermore, we demonstrated that NEAT1 positively regulated ATF2 expression via sponging miR-26a-5p. Conclusion ATF2 and NEAT1 form a positive feedback loop mediated by miR-26a-5p and coordinately contribute to LUAD progression.

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“…Moreover, Sev was found to diminish NEAT1, which was enhanced in mice with myocardial I/R, by microarray analysis. NEAT1 has been most frequently studied in various cancer as an oncogene, including cervical cancer [22], colon cancer [23] as well as glioma [24] by regulating cell migration, proliferation along with drug resistance. Additionally, NEAT1 was upregulated in Parkinson's disease and conferred drug-inducible neuroprotection against oxidative stress [25].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding NEAT1 weakens the protective role of sevoflurane on myocardial ischemia/reperfusion injury by mediating the microRNA-140/RhoA axis

Rui¹,

Wang²,

Xu³

2020

Preprint

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Background: The inhaled Sevoflurane (Sev) has been implicated to protect myocardial tissues against ischemia/reperfusion (I/R)-evoked injury. Nevertheless, the detailed mechanisms of Sev‐mediated cardioprotection remain basically unknown. This study intends to examine the roles of nuclear enriched abundant transcript 1 (NEAT1), a long non-coding RNA (lncRNA) during the cardioprotection exerted by Sev.Methods: We initially performed I/R surgery in mice, and Sev treatment was given during the perfusion, followed by the determination of cardiac function, myocardial infarction area and myocardial apoptosis for the validation of the model. Then, we conducted lncRNA microarray analysis on Sev-treated hearts to find out lncRNAs with significant differences in expression. The changes of myocardial I/R injury were evaluated by echocardiography, TTC staining and TUNEL assay after establishing mice with NEAT1 upregulation. Afterwards, the targeting miRNA of NEAT1 and the targeting mRNA of the miRNA were screened out through StarBase and microarray analyses to carry out rescue experiments.Results: NEAT1 was downregulated in Sev-treated cardiomyocytes. Overexpression of NEAT1 weakened cardiac function, increased infarct size and increased apoptosis in the presence of Sev. NEAT1 bound to microRNA (miR)-140, which was significantly upregulated in Sev-treated cardiomyocytes. Inhibition of miR-140 expression weakened the cardiac function of Sev-treated mice, increased infarct size and cardiomyocyte apoptosis. miR-140 mediated the RhoA pathway, and the RhoA activity inhibition attenuated miR-140 effects on Sev protection.Conclusion: Sev mitigates myocardial I/R injury by restoring NEAT1 expression and regulating the miR-140/RhoA axis.

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BCLAF1 promotes cell proliferation, invasion and drug-resistance though targeting lncRNA NEAT1 in hepatocellular carcinoma

Cited by 39 publications

References 26 publications

LncRNA NEAT1 remodels chromatin to promote the 5-Fu resistance by maintaining colorectal cancer stemness

LncRNA NEAT1 remodels chromatin to promote the 5-Fu resistance by maintaining colorectal cancer stemness

The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression

Long non-coding NEAT1 weakens the protective role of sevoflurane on myocardial ischemia/reperfusion injury by mediating the microRNA-140/RhoA axis

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