miR‑497 inhibits the proliferation and migration of A549 non‑small‑cell lung cancer cells by targeting FGFR1

Huang, Qibin; Li, Hongtao; Dai, Xiaofeng; Zhao, Di; Guan, Bingfeng; Wen, Xin

doi:10.3892/mmr.2019.10611

Cited by 9 publications

(9 citation statements)

References 37 publications

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“…The present study explored the expression of miR‐338 in the NSCLC. We demonstrated that the miR‐338 level was also down‐regulated in NSCLC tissues when compared with the adjacent normal tissues, which was consistent with previous results (Zhang, Shao, et al, ; Zhang, Ding, et al, ). In addition, the level of miR‐338 was also down‐regulated in NSCLC cell lines.…”

Section: Discussionsupporting

confidence: 92%

“…Lung cancer, one of the most frequently diagnosed cancers, leads to the largest number of cancer‐related deaths worldwide (Zhang, Shao, Lin, Liu, & Yang, ; Zhang, Ding, & Zhang, ). According to the recent data, we know that the 5‐year survival rate of patients with lung cancer is only 15%.…”

Section: Introductionmentioning

confidence: 99%

“…It is known that microRNAs (miRNAs) are participated in multiple biological processes including cell growth, migration, apoptosis, differentiation, inflammation, development, and stress response (Feng et al, ; Liu et al, ; Rothschild et al, ; Song et al, ; Wan, Zhang, Fan, & Wang, ). During past decades, a number of reports showed that miRNAs are either down‐regulated or up‐regulated, and play an important role in the carcinogenesis such as gastric cancer, gallbladder carcinoma, hepatocellular carcinoma, colorectal cancer, glioma, and bladder cancer (Feng et al, ; Garzon, Calin, & Croce, ; Li et al, ; Wang et al, ; Zhang, Shao, et al, ; Zhang, Ding, et al, ). Hence, studies of miRNAs in NSCLC are very critical to identify new diagnostic biomarker for lung cancer diagnosis.…”

Section: Introductionmentioning

confidence: 99%

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MiR‐338 regulates NFATc1 expression and inhibits the proliferation and epithelial‐mesenchymal transition of human non‐small‐cell lung cancer cells

2019

Molec Gen & Gen Med

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Background: It is well known that nuclear factor of activated T cells c1 (NFATc1) expression is closely associated with progression of many cancers. And we found that miR-338 could directly target the NFATc1. However, the precise mechanisms of miR-338 in non-small-cell lung cancer (NSCLC) have not been well clarified. Our study aimed to explore the interaction between NFATc1 and miR-338 in NSCLC. Methods: Quantitative RT-PCR was utilized to determine the expressions of NFATc1 and miR-338 in NSCLC tissues and cell lines. And the cell proliferation and epithelial-mesenchymal transition (EMT) were assessed to determine the functional roles of miR-338 and NFATc1 in NSCLC cells. NFATc1 expression was detected using quantitative RT-PCR and western blotting, respectively. Luciferase reporter assays were performed to validate NFATc1 as a target of miR-338 in NSCLC cells. Results: In this study, our results showed that NFATc1 expression was significantly up-regulated in NSCLC tissues and cell lines, and the miR-338 level was dramatically down-regulated. Moreover high NFATc1 expression was closely associated with low miR-338 level in NSCLC tissues. Moreover introduction of miR-338 significantly inhibited proliferation and EMT of NSCLC cells. Bioinformatics analysis predicted that the NFATc1 was a potential target gene of miR-338. We demonstrated that miR-338 could directly target NFATc1 by using luciferase reporter assay. Besides, knockdown of NFATc1 had the similar effects with miR-338 overexpression on NSCLC cells. Up-regulation of NFATc1 in NSCLC cells partially abolished the inhibitory effects of miR-338 mimic. Conclusions: Overexpression of miR-338 inhibited cell proliferation and EMT of NSCLC cells by directly down-regulating NFATc1 expression. K E Y W O R D S EMT, microRNA-338, NFATc1, NSCLC, proliferation 2 of 10 | HE and LU How to cite this article: He W, Lu J. MiR-338 regulates NFATc1 expression and inhibits the proliferation and epithelial-mesenchymal transition of human non-small-cell lung cancer cells. Mol Genet

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MiR‐338 regulates NFATc1 expression and inhibits the proliferation and epithelial‐mesenchymal transition of human non‐small‐cell lung cancer cells

2019

Molec Gen & Gen Med

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“…Pre-treatment with MAPK inhibitors reduced the protein expression of Bax promoted by IL-1α in the MC3T3-E1 cells, suggesting that the signi cance of JNK and the p38 MAPK signaling in modulating IL-1α-induced apoptosis and osteoblast differentiation of MC3T3-E1 cells [23]. The negative correlation between miR-497 and the JNK signaling has been highlighted in non-small cell lung cancer [24].…”

Section: Discussionmentioning

confidence: 96%

MicroRNA-497-5p stimulates osteoblast differentiation through HMGA2-mediated JNK signaling pathway

Zhao

Yang

Wang

et al. 2020

Preprint

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Background: Osteoporosis (OP) has the characteristics of the decline in bone mineral density and worsening of bone quality, contributing to higher risk of fractures. Some microRNAs (miRNAs) have been validated as possible mediators of osteoblast differentiation. We herein aimed to clarify whether miR-497-5p regulates differentiation of osteoblasts in MC3T3-E1 cells.Methods: The expression of miR-497-5p in OP patients and controls was measured by RT-qPCR, and its expression changes during osteoblast differentiation were determined as well. The effects of miR-497-5p on differentiation of MC3T3-E1 cells were studied using MTT, ALR staining and ARS staining. The target gene of miR-497-5p was predicted by TargetScan, and the effects of its target gene on differentiation and the pathway involved were investigated.Results: miR-497-5p expression expressed poorly in OP patients and its expression was upregulated during MC3T3-E1 cell differentiation. Overexpression of miR-497-5p promoted mineralized nodule formation and the expression of RUNX2 and OCN. miR-497-5p targeted high mobility group AT-Hook 2 (HMGA2), while upregulation of HMGA2 inhibited osteogenesis induced by miR-497-5p mimic. miR-497-5p significantly impaired the c-Jun NH2-terminal kinase (JNK) pathway, whereas HMGA2 activated this pathway. Activation of the JNK pathway inhibited the stimulative role of miR-497-5p mimic in osteogenesis.Conclusions: miR-497-5p inhibits development of OP by hampering osteogenesis via targeting HMGA2. We hence conclude that targeting miR-497-5p might be an attractive therapeutic option for OP.

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“…27 Moreover, Huang et al suggested that miR-497 could act as a tumor suppressor in NSCLC to hinder the proliferation and migration of NSCLC cells. 28 For miR-25-3p, Ding et al reported that miR-25 could promote the migration and invasion of NSCLC. 20 Also, Xiang et al suggested that miR-25 was related to the proliferation and motility of NSCLC.…”

Section: Discussionmentioning

confidence: 99%

<p>Hsa_circ_0043265 Suppresses Proliferation, Metastasis, EMT and Promotes Apoptosis in Non-Small Cell Lung Cancer Through miR-25-3p/FOXP2 Pathway</p>

Ren¹,

Liu²,

Hou³

et al. 2020

OTT

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Purpose: Non-small cell lung cancer (NSCLC) is the largest type of lung cancer (LC) with a higher mortality rate. Circular RNAs (circRNAs) have been shown to play an important role in cancer progression. Therefore, this study was to explore the function of hsa_circ_0043265 in NSCLC. Methods: The expression levels of hsa_circ_0043265, microRNA-25-3p (miR-25-3p) and forkhead box P2 (FOXP2) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Ribonuclease R (RNase R) and Actinomycin D (ActD) were used to verify the authenticity and stability of hsa_circ_0043265. Cell counting kit-8 (CCK-8), flow cytometry and transwell assays were used to evaluate the abilities of proliferation, apoptosis, migration and invasion of NSCLC cells. Also, Western blot (WB) analysis was performed to assess the levels of apoptosis, epithelial-mesenchymal transition (EMT) and proliferationrelated proteins and FOXP2 protein. RNA immunoprecipitation (RIP) and dual-luciferase reporter assays were used to verify the interaction between miR-25-3p and hsa_circ_0043265 or FOXP2. Besides, mice xenograft models were constructed to confirm the effect of hsa_circ_0043265 on NSCLC tumor growth in vivo. Results: Hsa_circ_0043265 was lowly expressed in NSCLC tissues and cells, and its overexpression inhibited the proliferation, migration, invasion and EMT process, while improved the apoptosis of NSCLC cells. MiR-25-3p could be sponged by hsa_circ_0043265, and its overexpression could invert the suppression effect of overexpressed-hsa _circ_0043265 on NSCLC progression. Moreover, FOXP2 was a target of miR-25-3p, and its silencing also could reverse the inhibition effect of overexpressed-hsa_circ_0043265 on NSCLC progression. In addition, hsa_circ_0043265 overexpression reduced the tumor growth of NSCLC in vivo. Conclusion: Hsa_circ_0043265 could sponge miR-25-3p to improve FOXP2 expression, thereby inhibiting NSCLC progression. This study showed that hsa_circ_0043265 could be a potential biomarker for early diagnosis of NSCLC.

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miR‑497 inhibits the proliferation and migration of A549 non‑small‑cell lung cancer cells by targeting FGFR1

Cited by 9 publications

References 37 publications

MiR‐338 regulates NFATc1 expression and inhibits the proliferation and epithelial‐mesenchymal transition of human non‐small‐cell lung cancer cells

MiR‐338 regulates NFATc1 expression and inhibits the proliferation and epithelial‐mesenchymal transition of human non‐small‐cell lung cancer cells

MicroRNA-497-5p stimulates osteoblast differentiation through HMGA2-mediated JNK signaling pathway

<p>Hsa_circ_0043265 Suppresses Proliferation, Metastasis, EMT and Promotes Apoptosis in Non-Small Cell Lung Cancer Through miR-25-3p/FOXP2 Pathway</p>

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