Downregulated miR‐144‐3p contributes to progression of lung adenocarcinoma through elevating the expression of <i>EZH2</i>

Liu, Chao; Yang, Zuozhang; Deng, Zhiyong; Zhou, Youjun; Gong, Quan; Zhao, Ruilian; Chen, Ting

doi:10.1002/cam4.1714

Cited by 30 publications

(34 citation statements)

References 25 publications

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“…Recent years, the expression status and biological function of miR-144-3p have been intensively investigated in many cancers [9,[20][21][22]. However, previous studies have produced inconsistent results.…”

Section: Discussionmentioning

confidence: 99%

“…For example, Yin reported that miR-144-3p is downregulated in breast cancer and functions as a tumor suppressor through repressing CEP55 [9]. Liu et al showed that the expression of miR-144-3p is decreased in lung adenocarcinoma (LUAD) tissues, and overexpression of miR-144-3p inhibited propagation and invasiveness of LUAD cells [20]. In contrast, other groups reported that miR-144-3p is upregulated in the specimens of nasopharyngeal carcinoma and clear cell renal cell carcinoma and serves as an onco-miRNA [21,22].…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-144-3p Inhibits Tumorigenesis of Oral Squamous Cell Carcinoma by downregulating ERO1L

Jiang

et al. 2020

J. Cancer

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An increasing number of studies indicate that miR-144-3p is dysregulated in numerous cancers, but its role in oral squamous cell carcinoma (OSCC) remains largely unknown. Herein we demonstrated that miR-144-3p expression was significantly downregulated in OSCC tissues and cell lines. Moreover, the low level of miR-144-3p expression was associated with the clinical characteristics of OSCC patients. Furthermore, ectopic expression of miR-144-3p inhibited the proliferation, migration, and invasion of OSCC cells in vitro, and blunted the tumorigenic ability of OSCC cells in vivo. Additionally, the levels of miR-144-3p were negatively correlated with the expression status of endoplasmic reticulum oxidoreduction-1-like (ERO1L) in OSCC cell lines. Subsequently, we identified that ERO1L was a direct target of miR-144-3p. Intriguingly, we found that miR-144-3p downregulation of ERO1L inhibited the activity of signal transducer and activator of transcription 3 (STAT3) in OSCC cells. Therefore, miR-144-3p suppresses tumorigenesis by targeting ERO1L/STAT3 signaling pathway in OSCC. miR-144-3p may a candidate target for OSCC treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA-144-3p Inhibits Tumorigenesis of Oral Squamous Cell Carcinoma by downregulating ERO1L

Jiang

et al. 2020

J. Cancer

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“…In LUAD, oncogenic networks and oncogenes guided by miR-143 were identified and may help with tumor suppressor effects, establish new prognostic indicators, and find therapeutic targets [17]. The propagation, migration, and invasion of LUAD cells are obstructed by overexpression of the miR-144 family target, EZH2 [18]. These studies all indicate that miRNAs in the ceRNA network may act as suppressors in LUAD.…”

Section: Discussionmentioning

confidence: 94%

A signature related to lung adenocarcinoma prognosis: A study based on TCGA database

Wang¹,

Zhang²,

Zhang³

et al. 2020

Preprint

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Background: The intrinsic molecular subtypes of lung adenocarcinoma (LUAD) impact clinical treatment decision-making, but the molecular mechanisms are still unclear. Therefore, we aimed to identify sensitive biomarkers to evaluate LUAD patient prognosis. Methods: Differentially expressed RNAs from LUAD patients were obtained from The Cancer Genome Atlas (TCGA) database and they were used to construct a competitive endogenous RNA (ceRNA) network. Based on the examination of clinical data, long noncoding RNAs (lncRNAs) and mRNAs in the network were selected by univariate and multivariate Cox regression analysis. Finally, functional enrichment analysis was used to reveal prognostic signatures based on the classification into high and low-risk groups, survival analysis, and an independence test. Results: The ceRNA network consisted of 21 mRNAs, 53 lncRNAs, and 8 miRNAs that were selected from the differentially expressed RNAs identified. Next, based on univariate and multivariate Cox regression analysis, a prognostic signature, including two mRNAs (HOXA10 and CBX2) and four lncRNAs (LINC00460, LINC00330, DGCR5, and C14orf132) was constructed. Eventually, survival analysis showed that significant differences in survival rates between high and low-risk groups and the area under the curve (AUC) for three‐year survival was 0.714. Compared with clinical risk factors, including age, pathological stage, and TNM stage, our risk score had a higher prognostic value. Conclusion: By screening from a ceRNA network, we constructed a signature, including two mRNAs (HOXA10 and CBX2) and four lncRNAs (LINC00460, LINC00330, DGCR5, and C14orf132), that can be utilized as a prognostic biomarker in LUAD. This signature may provide options for clinical treatment.

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“…MiR-144-5p increased the radiosensitivity of NSCLC cells by repressing activating transcription factor 2 (ATF2) [45] and miR-451a decreased doxorubicin resistance in lung cancer via suppressing c-Myc [46]. MiR-144-3p and MiR-30a-3p inhibited the progression of lung cancer via targeting EZH2 and DNA methyltransferase 3a [47,48]. Long noncoding RNA RMRP sponged miR-1-3p to promote NSCLC cell proliferation and invasion [49].…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel Transcription Factor-microRNA-mRNA Co-regulatory Networks in Pulmonary Large-cell Neuroendocrine Carcinomas

Cai

Zhang

2020

Preprint

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Background: Large-cell neuroendocrine carcinoma (LCNEC) of the lung is a rare neuroendocrine neoplasm. Previous studies have shown that microRNAs can be widely involved in tumor regulation through targeting critical genes. However, it is unclear about which miRNAs play vital roles in LCNEC’s pathogenesis and how they interact with transcription factors (TFs) to regulate the cancer-related genes. Methods: To clarify the new TFs-miRNA-target gene feed-forward loops (FFLs) model of LCNEC, we integrated multi-omics data from GEO, TRRUST, TRED, and miRTarBase database. First, expression profile datasets for mRNAs (GSE1037) and miRNAs (GSE19945) were downloaded from the GEO database. Overlapping differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs) were identified through integrative analysis. The target genes of the FFL being obtained from the mirTarBase database, the GO and KEGG functional enrichment analysis was performed on the target gene. Then, we screened for key miRNAs in the FFL and perform gene regulatory network analysis based on key miRNAs. Finally, the TF-miRNA-target gene FFLs were constructed by the hypergeometric test.Results: A total of 343 DEGs and 60 DEMs were identified in LCNECs compared to normal tissues, including 210 downregulated, 133 upregulated genes and 29 downregulated, 31 upregulated miRNAs. Additionally, 55 DEMs were predicted through miRanda, mirDB, and TargetScan to be associated with the LCNEC 77 key genes. Finally, ETS1-miR195-CD36 and E2F3-miR195-CD36 from the TF-miRNA-mRNA FFLs were constructed and are significantly enriched in focal adhesion, cytokine-receptor interaction, hematopoietic cell lineage, and transforming growth factor (TGF)-β signaling pathways. Survival analysis showed that the differential expression of the multi-effect factors ETS1, CD36, and hsa-miR-195 in the FFL significantly affected the survival time of LCNEC patients.Conclusion: In summary, we construct the TF-miRNA-target regulatory network, which is helpful to understand the complex LCNEC regulatory mechanisms. The expression difference of regulated multi-effect target factors ETS1, CD36, and hsa-miR-195 has a significant impact on the survival and development of LCNEC.

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Downregulated miR‐144‐3p contributes to progression of lung adenocarcinoma through elevating the expression of EZH2

Cited by 30 publications

References 25 publications

MicroRNA-144-3p Inhibits Tumorigenesis of Oral Squamous Cell Carcinoma by downregulating ERO1L

MicroRNA-144-3p Inhibits Tumorigenesis of Oral Squamous Cell Carcinoma by downregulating ERO1L

A signature related to lung adenocarcinoma prognosis: A study based on TCGA database

Identification of Novel Transcription Factor-microRNA-mRNA Co-regulatory Networks in Pulmonary Large-cell Neuroendocrine Carcinomas

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