MiR-4319 hinders YAP expression to restrain non-small cell lung cancer growth through regulation of LIN28-mediated RFX5 stability

Yang, Yi; He, Ling; Liu, Yü; Chi, Chuang; Ni, Jiangwei; Liu, Xiaoming

doi:10.1016/j.biopha.2019.108956

Cited by 27 publications

(19 citation statements)

References 24 publications

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“…It is known that dysregulation of specific miRNAs can be involved in the initiation and progression of cancer (23). Various miRNAs have been reported to function as oncogenes or tumor suppressors in NSCLC by regulating the expression of downstream target genes (24,25). A previous study revealed that miR-671-5p served tumor suppressor roles in breast cancer; overexpression of miR-671-5p attenuated the proliferation and invasion of breast cancer cells by targeting FOXM1 (26).…”

Section: Discussionmentioning

confidence: 99%

Upregulated microRNA‑671‑3p promotes tumor progression by suppressing forkhead box P2 expression in non‑small‑cell lung cancer

Zhang

et al. 2019

Mol Med Report

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In the present study, the expression of microRNA (miR)-671-3p in non-small-cell lung cancer (NSCLC) was detected via reverse transcription-quantitative polymerase chain reaction analysis, and its role in cell proliferation, apoptosis, migration and invasion was investigated via Cell Counting Kit-8, colony formation, flow cytometry, Transwell and scratch assays, respectively. It was observed that the expression of miR-671-3p was upregulated in NSCLC tissues and cell lines (A549 and H1975). Treatment with miR-671-3p inhibitors suppressed cell proliferation, migration and invasion, and increased apoptosis in vitro, suggesting that miR-671-3p functions as an oncogene in NSCLC. In addition, forkhead box P2 (FOXP2) has been reported to be a tumor suppressor that is downregulated in several types of cancer, and its low expression was confirmed in NSCLC tissues and cell lines in the current study via western blotting. The results of the luciferase reporter assay also demonstrated that miR-671-3p targeted directly the 3′-untranslated region of FOXP2. Furthermore, overexpression of FOXP2 in A549 and H1975 cell lines suppressed the growth, migration and invasion, and promoted apoptosis, whereas these effects were reversed by transfection with miR-671-3p mimics, suggesting that miR-671-3p promoted tumor progression via regulating FOXP2. Taken together, the results reported in the present study implied that miR-671-3p may be a potential therapeutic target in NSCLC.

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Section: Discussionmentioning

confidence: 99%

Upregulated microRNA‑671‑3p promotes tumor progression by suppressing forkhead box P2 expression in non‑small‑cell lung cancer

Zhang

et al. 2019

Mol Med Report

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“…Over 2,000 miRNA genes have been identified in the human genome; these miRNAs are estimated to regulate approximately 30% of all protein-coding genes [19]. Aberrations in the expression of miRNAs involved in tumor-suppressive or oncogenic processes have been widely reported in NSCLC [20][21][22]. Therapies that target lncRNAs and/or miRNAs may be potentially used for effective NSCLC management.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA VPS9D1-AS1 augments the malignant phenotype of non-small cell lung cancer by sponging microRNA-532-3p and thereby enhancing HMGA2 expression

Han

Huang

Han

2020

Aging

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We investigated the influence of the long noncoding RNA VPS9D1 antisense RNA 1 (VPS9D1-AS1) on the malignant phenotype of non-small cell lung cancer (NSCLC) cells in vitro and in vivo. We also explored the mechanisms by which VPS9D1-AS1 exerts its oncogenic action during NSCLC progression. VPS9D1-AS1 expression was upregulated in NSCLC; the extent of its upregulation significantly correlated with patients' adverse clinicopathological characteristics and shorter overall survival. When VPS9D1-AS1 was knocked down in NSCLC cells, their proliferation, colony-forming capacity, migration, and invasiveness were lower, whereas their apoptosis rate was higher, compared to the control. VPS9D1-AS1 knockdown attenuated tumor growth of NSCLC cells in vivo. Mechanistically, VPS9D1-AS1 directly interacted with microRNA-532-3p (miR-532-3p) in NSCLC cells; the impact of VPS9D1-AS1 knockdown on NSCLC cells was attenuated by miR-532-3p inhibition. Furthermore, VPS9D1-AS1 knockdown decreased the expression of high mobility group AThook 2 (HMGA2) in NSCLC cells via miR-532-3p sponging. Recovery of HMGA2 expression partially reversed the inhibitory effects of VPS9D1-AS1 knockdown on NSCLC cells. Thus, VPS9D1-AS1 functions as a competing endogenous RNA that positively regulates HMGA2 expression by sponging miR-532-3p in NSCLC cells, suggesting that the VPS9D1-AS1-miR-532-3p-HMGA2 pathway can be a potential diagnostic and/or therapeutic target in NSCLC.

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“…Previous studies have revealed that miR-4319 elicits inhibitory effects on the proliferation of breast cancer and prostate cancer 22, 23, and miR-4319 could repress cancer stemness in triple-negative breast cancer through targeting E2F2 22. MiR-4319 also exhibits tumour suppressor activities in NSCLC (non-small-cell lung cancer) through targeting LIN28/RFX5/YAP cascades to mitigate cell migration and proliferation and facilitate cell apoptosis 24. Moreover, miR-4319 is transcriptionally modulated by PLZF and acts as a tumour suppressor in CRC (colorectal cancer) via targeting ABTB1 21.…”

Section: Introductionmentioning

confidence: 99%

MiR-4319 induced an inhibition of epithelial-mesenchymal transition and prevented cancer stemness of HCC through targeting FOXQ1

et al. 2019

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The heterogeneity existing in tumours is responsible for the poor response to treatment. Therefore, elucidating the molecular mechanisms of intratumoural heterogeneity in hepatocellular carcinoma (HCC) is vital for the discovery of new therapeutic methods for improving the prognosis of patients. Of note, cancer stem cells (CSCs) existing in HCC may explain the pathological properties of heterogeneity and recurrence. An increasing number of studies have confirmed that abnormally expressed microRNAs (miRNAs) take part in the carcinogenesis as well as the aggravation of HCC. However, little information is currently available about the specific miR-4319 in HCC. Herein, we demonstrated that the level of miR-4319 was remarkably decreased in HCC specimens and cells compared to that in normal counterparts and that the depression of miR-4319 in tumour specimens correlates with tumour size, histological grade and venous invasion. Through a series of functional experiments, we illustrated that miR-4319 repressed cell proliferation, accelerated apoptosis, inhibited epithelial-mesenchymal transition (EMT) and prevented cancer stemness in HCC cells by targeting FOXQ1 (Forkhead box Q1). An in vivo tumourigenesis assay uncovered that depletion of miR-4319 in Hep3B cells increased tumour growth and elevated the expression of EMT and CSC markers in comparison to those of the control group. Restoration of FOXQ1 expression also partially reversed the miR-4319-induced biological effects on HCC cells. Thus, miR-4319, as a posttranscriptional regulator, plays a profound role in suppressing the malignant progression of HCC, and our study highlights the miR-4319/FOXQ1 cascade as a potential therapeutic target for conquering HCC.

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MiR-4319 hinders YAP expression to restrain non-small cell lung cancer growth through regulation of LIN28-mediated RFX5 stability

Cited by 27 publications

References 24 publications

Upregulated microRNA‑671‑3p promotes tumor progression by suppressing forkhead box P2 expression in non‑small‑cell lung cancer

Upregulated microRNA‑671‑3p promotes tumor progression by suppressing forkhead box P2 expression in non‑small‑cell lung cancer

Long noncoding RNA VPS9D1-AS1 augments the malignant phenotype of non-small cell lung cancer by sponging microRNA-532-3p and thereby enhancing HMGA2 expression

MiR-4319 induced an inhibition of epithelial-mesenchymal transition and prevented cancer stemness of HCC through targeting FOXQ1

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