Genetic and epigenetic silencing of mircoRNA-506-3p enhances COTL1 oncogene expression to foster non-small lung cancer progression

Guo, Shuai; Yang, Peiying; Jiang, Xingkang; Li, Xiaojiang; Wang, Yuan‐Yuan; Zhang, Xin; Sun, Binxu; Zhang, Yao; Jia, Yulin

doi:10.18632/oncotarget.13501

Cited by 50 publications

(41 citation statements)

References 39 publications

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“…The results of the present study demonstrated a decrease in the miR-506-3p expression levels in PC-9GR cells, as compared with those in the parental cells. The cell proliferation assay demonstrated that miR-506-3p mimics inhibited the growth of both PC-9GR and PC-9 cells compared with miR-NC mimics, which is consistent with the findings of a previous study on the anti-proliferative function of miR-506-3p in NSCLC cells (22). Notably, the overexpression of miR-506-3p markedly increased the cell viability reduction and apoptosis following gefitinib treatment in PC-9GR cells, while the inhibition of miR-506-3p was demonstrated to have the opposing effect.…”

Section: Discussionsupporting

confidence: 90%

“…Yin et al (21) reported that miR-506-3p was upregulated in lung cancer tissue in 83% of patients with lung cancer; however, the elevation in miR-506-3p expression inhibited tumor growth in lung cancer cells in vivo (17). Another recent study detected miR-506-3p downregulation in NSCLC and revealed that miR-506-3p inhibited NSCLC progression (22). In the present study, the downregulation of miR-506-3p expression in NSCLC was confirmed, and the role of miR-506-3p in mediating gefitinib sensitivity in NSCLC cells was identified.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑506‑3p reverses gefitinib resistance in non‑small cell lung cancer by targeting Yes‑associated protein 1

2018

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Epidermal growth factor receptor-tyrosine kinase inhibitors, such as gefitinib, have been found to be clinically effective in the treatment of patients with non-small cell lung cancer (NSCLC). However, the therapeutic effect of gefitinib is often limited by the development of gefitinib resistance. MicroRNAs (miRNAs), a group of small non-coding RNAs, have been demonstrated to be frequently dysregulated in human malignancies. For instance, the downregulation of miR-506-3p has been reported in NSCLC patients. The aim of the present study was to determine the role and underlying molecular mechanism of miR-506-3p in the regulation of gefitinib sensitivity in NSCLC. A gefitinib-resistant PC-9 (PC-9GR) cell line was established, and reduced miR-506-3p expression was observed in PC-9GR cells as compared with that in parental cells. The results of cell cytotoxicity and cell apoptosis assays indicated that PC-9GR cells were more sensitive to gefitinib following the transfection with an miR-506-3p mimic, while transfection with an miR-506-3p antagonist reduced the sensitivity of PC-9GR cells to gefitinib. It was further revealed that Yes-associated protein 1 (YAP1) was directly suppressed by miR-506-3p in PC-9GR cells. The elevated sensitivity of PC-9GR cells to gefitinib following transfection with the miR-506-3p mimic was counteracted by the overexpression of YAP1. Furthermore, an inverse correlation between the miR-506-3p and YAP1 mRNA levels was detected in lung adenocarcinoma specimens. Collectively, the results of the present study suggested that the downregulation of miR-506-3p contributes to gefitinib resistance, and thus, the restoration of miR-506-3p may be a potential therapeutic approach for overcoming NSCLC gefitinib resistance.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

MicroRNA‑506‑3p reverses gefitinib resistance in non‑small cell lung cancer by targeting Yes‑associated protein 1

2018

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“…Both UCA1 silencing and miR-143 overexpression could cause a significant decrease of mitogen-activated protein kinase 1 (MAPK1) [92]. Similarly, UCA1 contributed to proliferation and invasion of non-small cell lung cancer by functioning as a ceRNA to miR-506-3p, up-regulating its direct downstream target, coactosin-like protein 1 (COTL1) [93].…”

Section: Lung Cancermentioning

confidence: 99%

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Xuan

Zhang

et al. 2019

FEBS Letters

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Long non-coding RNAs (lncRNAs) are a major subset of highly conserved non-coding RNAs (ncRNAs) that consist of at least 200 nucleotides and have limited protein-coding potential. Cumulative data have shown that lncRNAs are deregulated in many types of cancer and may control pathophysiological processes of cancer at various levels, including transcription, post-transcription and translation. Recently, lncRNAs have been demonstrated to interact with microRNAs (miRNAs), another major subset of ncRNAs, which regulate physiological and pathological processes by inhibiting target mRNA translation or promoting mRNA degradation. The lncRNA urothelial carcinomaassociated 1 (UCA1) has recently gained much attention as it is overexpressed in many types of cancer and is involved in carcinogenesis. Here, we review the crosstalk between UCA1 and miRNAs during the pathogenesis of cancer, with a focus on cancer-cell proliferation, invasion, drug resistance, and metabolism.

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“…Has-miR-1270 was reported to interacted with circRNAs to regulate the tumorigenesis and development of LADC [40] and the cell invasion and migration in NSCLC [41]. Has-miR-506-3p was identi ed as a tumor suppressor in several cancers, including NSCLC [42] and colorectal cancer [43]. It can also reverse ge tinib resistance in NSCLC by targeting Yes-associated protein 1 [44].…”

Section: Discussionmentioning

confidence: 99%

Identification of LINC02310 as an enhancer in lung adenocarcinoma and investigation of its regulatory network via comprehensive analyses

Zhao

Wang

Luo

et al. 2020

Preprint

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Background: Lung adenocarcinoma (LADC) is a major subtype of non-small cell lung cancer (NSCLC) and has one of the highest mortality rates. An increasing number of long non-coding RNAs (LncRNAs) were reported to be associated with the occurrence and progression of LADC. Thus, tt is necessary and reasonable to find new prognostic biomarkers for LADC among LncRNAs.Methods: Differential expression analysis, survival analysis, PCR experiments and clinical feature analysis were performed to screen out the LncRNA which was significantly related to LADC. Its role in LADC was verified by CCK-8 assay and colony. Furthermore, competing endogenous RNA (ceRNA) regulatory network construction, enrichment analysis and protein-protein interaction (PPI) network construction were performed to investigate the downstream regulatory network of the selected LncRNA.Results: A total of 2431 differentially expressed LncRNAs (DELncRNAs) and 2227 differentially expressed mRNAs (DEmRNAs) were from The Cancer Genome Atlas (TCGA) database. Survival analysis results indicated that lnc-YARS2-5, lnc-NPR3-2 and LINC02310 were significantly related to overall survival. Their overexpression indicated poor prognostic. PCR experiments and clinical feature analysis suggested that LINC02310 was significantly correlated with TNM-stage and T-stage. CCK-8 assay and colony formation assay demonstrated that LINC02310 acted as an enhancer in LADC. In addition, 3 targeted miRNAs of LINC02310 and 414 downstream DEmRNAs were predicted. The downstream DEmRNAs were then enriched in 405 Gene Ontology (GO) terms and 11 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, which revealed their potential functions and mechanisms. The PPI network showed the interactions among the downstream DEmRNAs. Conclusions: This study verified LINC02310 as an enhancer in LADC and performed comprehensive analyses on its downstream regulatory network, which might benefit LADC prognoses and therapies.

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Genetic and epigenetic silencing of mircoRNA-506-3p enhances COTL1 oncogene expression to foster non-small lung cancer progression

Cited by 50 publications

References 39 publications

MicroRNA‑506‑3p reverses gefitinib resistance in non‑small cell lung cancer by targeting Yes‑associated protein 1

MicroRNA‑506‑3p reverses gefitinib resistance in non‑small cell lung cancer by targeting Yes‑associated protein 1

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Identification of LINC02310 as an enhancer in lung adenocarcinoma and investigation of its regulatory network via comprehensive analyses

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