LncRNA DLEU2 accelerates the tumorigenesis and invasion of non–small cell lung cancer by sponging miR‐30a‐5p

Wu, Weiming; Zhao, Yongliang; Gao, Erji; Yang, Li; Guo, Xiang; Zhao, Tong; He, Weiwei; Zhang, Huibiao

doi:10.1111/jcmm.14749

Cited by 43 publications

(38 citation statements)

References 27 publications

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“…LncRNA plays a key role in many types of diseases, including cancer, cardiovascular disease, autoimmune diseases, and nervous system diseases (Yang et al, 2014). Recently, more and more studies suggest that lncRNA may be closely related to leukemia (Gourvest et al, 2019;Wu et al, 2019). However, the role of lncRNA in the proliferation and differentiation of leukemia cells induced by ATPR is unclear.…”

Section: Introductionmentioning

confidence: 99%

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

Feng

et al. 2020

Front. Cell Dev. Biol.

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Abundant evidence has illustrated that long non-coding RNA (lncRNA) plays a vital role in the regulation of tumor development and progression. Most lncRNAs have been proven to have biological and clinical significance in acute myeloid leukemia (AML), but further investigation remains necessary. In this study, we investigated lncRNA NR-104098 in AML and its specific mechanism. The microarray analysis was performed on NB4 cells. Based on the related analysis results, we identified that lncRNA NR-104098 is a suppressor gene that is significantly upregulated in AML cells. LncRNA NR-104098 could inhibit proliferation and induce differentiation in AML cells in vitro and also play main role in the mouse xenografts. Mechanically, it was confirmed that lncRNA NR-104098 may effectively inhibit EZH2 transcription by directly binding to E2F1 and recruiting E2F1 to the EZH2 promoter. In addition, ATPR can significantly increase the expression of lncRNA NR-104098, whereas knocking down NR104098 can inhibit the inhibitory effect of ATPR on the proliferation and induction differentiation of AML cells. Taken together, these results lead to deeper insight into the mechanism of ATPR-induced AML differentiation and prevent proliferation by inhibiting EZH2 on the transcriptional level.

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Section: Introductionmentioning

confidence: 99%

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

Feng

et al. 2020

Front. Cell Dev. Biol.

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“…As a new noncoding RNA molecule, the abnormal expression of lncRNA in tumor tissue has attracted extensive attention of researchers [23,28]. Many studies have shown that lncRNA is likely to be a carcinogen gene [18,19] or a tumor suppressor gene [18] in the occurrence and development of tumors, and has increasingly become a biomarker of tumor diagnosis, treatment or prognosis, including AML [15,36]. Therefore, it is very important to identify more new cancer related lncRNAs and explore their biological functions and molecular mechanisms in order to explore new therapeutic methods of AML.…”

Section: Introductionmentioning

confidence: 99%

lncRNA HOXA-AS2 functions as an oncogene by binding to EZH2 and suppressing LATS2 in Acute myeloid leukemia (AML)

Feng

et al. 2020

Preprint

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BackgroundLong noncoding RNAs (lncRNAs) plays an important role in the development of physiology and pathology. Many reports have shown that lncRNA HOXA cluster antisense RNA 2 (HOXA-AS2) is a carcinogen and plays an important role in many tumors, but little is known about its role in Acute myeloid leukemia (AML). MethodsThe expression of HOXA-AS2 in AML cell line was detected by qRT-PCR. AML cases from the public database (GEPIA) were also included in this study. Cell counting kit-8 (CCK-8) assay, flow cytometry, immunofluorescence and Western blot were used to detect the role of HOXA-AS2 in AML cells. Luciferase reporter gene detection, RIP, RNA pull-down and RNA-ChIP detection were used to demonstrate the molecular biological mechanism of HOXA-AS2 in AML.ResultsHOXA-AS2 was upregulated in AML cell lines and tissues, and the overexpression of HOXA-AS2 is negatively correlated with the survival of patients. Silencing HOXA-AS2 can inhibit the proliferation and induce differentiation of AML cells in vitro and in vivo. Overexpressing HOXA-AS2 showed the opposite result. Moreover, more in-depth mechanism studies showed that carcinogenicity of HOXA-AS2 exerted mainly through binding with the epigenetic inhibitor Enhancer of zeste homolog 2 (EZH2) and then inhibiting the expression of Large Tumor Suppressor 2 (LATS2). ConclusionsTaken together, our findings highlight the important role of HOXA-AS2 in AML, suggesting that HOXA-AS2 may be an effective therapeutic target for patients with AML.

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“…LncRNAs, which are encoded by an unstudied region of the human genome, may contain cancer-missing drivers and have attracted attention in recent years as potentially important regulators of carcinogenesis and cancer development. Increasing evidence has indicated that lncR-NAs play an important role in various human diseases, especially in malignant tumors [21][22][23][24]. Antisense long non-coding RNAs, such as TTN-AS1, IDH1-AS1 and AFAP-AS1, have been reported in tumors and closely related to the prognosis, development, invasion and metastasis of tumors [25][26][27].…”

Section: Discussionmentioning

confidence: 99%

The clinical prognostic value of lncRNA FAM83H-AS1 in cancer patients: a meta-analysis

Yang¹,

Wang²,

Zhong³

et al. 2020

Cancer Cell Int

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Background: Family with sequence similarity 83 member H antisense RNA 1 (FAM83H-AS1) is a novel long noncoding RNA. Increasing studies have reported that FAM83H-AS1 is abnormally expressed in a variety of tumors and is associated with poor outcome. However, the clinical prognostic significance of lncRNA FAM83H-AS1 in tumors is not completely known. Methods:In this meta-analysis, literature was collected up until February 5, 2020 through multifarious retrieval strategies by searching through electronic databases of PubMed, Cochrane Library, EMBASE, Medline, Web of Science, CNKI, Weipu, and Wanfang. A total of 14 studies that met the inclusion criteria with relevant clinical data and prognostic information were included in the meta-analysis. Results:The combined results revealed that high expression of FAM83H-AS1 was associated with poor overall survival (OS) (HR = 1.63, 95% CI 1.24-2.14, P = 0.0004) in a variety of cancers. Additionally, upregulated FAM83H-AS1 expression was significantly correlated with tumor TNM stage (III/IV vs. I/II, OR = 2.40, 95% CI 1.36-4.23, P = 0.003) and lymph node metastasis (positive vs. negative, OR = 1.70, 95% CI 1.14-2.52, P = 0.008) in patients with cancer. Conclusions:Our results of this meta-analysis indicated that elevated FAM83H-AS1 expression could predict poor prognosis in patients with cancer and suggested that FAM83H-AS1 might serve as a novel biomarker for cancer.

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LncRNA DLEU2 accelerates the tumorigenesis and invasion of non–small cell lung cancer by sponging miR‐30a‐5p

Cited by 43 publications

References 27 publications

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

lncRNA HOXA-AS2 functions as an oncogene by binding to EZH2 and suppressing LATS2 in Acute myeloid leukemia (AML)

The clinical prognostic value of lncRNA FAM83H-AS1 in cancer patients: a meta-analysis

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