Enhanced plasma miR‑26a‑5p promotes the progression of bladder cancer via targeting PTEN

Wang, Hui; Hu, Zhao; Chen, Li

doi:10.3892/ol.2018.9163

Cited by 16 publications

(16 citation statements)

References 27 publications

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“…Significantly growth inhibition was found in estrogen stimulated tumor xenograft models and ER+ breast cancer cells when up-regulating miR-26a expression [30]. Moreover, some researches demonstrated miR-26a-5p may also indirectly promote initiation and progression of some cancers [20,31,32]. Up-regulated expression of miR-26a was observed in gastric cancer cells MKN-28 and promoted cells proliferation, migration and invasion [32].…”

Section: Discussionmentioning

confidence: 99%

MiR-26a-5p enhances cells proliferation, invasion, and apoptosis resistance of fibroblast-like synoviocytes in rheumatoid arthritis by regulating PTEN/PI3K/AKT pathway

Huang

Xing

et al. 2019

Bioscience Reports

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Behavior alterations in fibroblast-like synoviocytes (FLS) contribute to a pivotal role in pathogenesis of rheumatoid arthritis (RA). MiRNAs are closely involved in a variety of pathologic conditions. In the present study, we aimed to screen for the aberrant expression of miRNAs in rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) to further identify the altered expression of miR-26a-5p in RA-FLS and to investigate the role of miR-26a-5p in RA. The altered expression of miR-26a-5p in RA-FLS was screened by microarray analysis and confirmed by quantitative real time PCR. The effect of miR-26a-5p on proliferation, cell cycle, apoptosis, and invasion in RA-FLS were studied. The verification of miR-26a-5p target mRNA and downstream signaling pathway was elucidated by bioinformatics analysis, dual luciferase reporter assay, and western blot. Expression of miR-26a-5p was higher in RA-FLS than in fibroblast-like synoviocytes from osteoarthritis patients and trauma patients. Overexpression of miR-26a-5p RA-FLS promoted cells proliferation, G1/S transition, cells invasion, and resisted apoptosis in RA-FLS, whereas it led to contrary effects when inhibiting the expression of miR-26a-5p. The 3′UTR of tensin homolog (PTEN) was directly targetted by miR-26a-5p and activation of phosphoinositide 3-kinase (PI3K)/AKT pathway was observed when overexpression of miR-26a-5p. Our study suggested that miR-26a-5p has a complementary role in cells proliferation, invasion, and apoptosis of RA-FLS, which may be attributed to its activation effect on PI3K/AKT signaling pathway via targetting PTEN. MiR-26a-5p is likely to be a clinically helpful target for novel therapeutic strategies in RA.

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Section: Discussionmentioning

confidence: 99%

MiR-26a-5p enhances cells proliferation, invasion, and apoptosis resistance of fibroblast-like synoviocytes in rheumatoid arthritis by regulating PTEN/PI3K/AKT pathway

Huang

Xing

et al. 2019

Bioscience Reports

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“…In addition, downregulation of PTEN by miR-26a-5p have been reported to promote the progression of bladder cancer. 27 – 29 Therefore, we propose that miR-26a-5p exhibits its effects not only through the regulation of FAF1 expression, but also by other means.…”

Section: Discussionmentioning

confidence: 99%

<p>MiR-26a-5p Serves as an Oncogenic MicroRNA in Non-Small Cell Lung Cancer by Targeting FAF1</p>

Ye¹,

Dong²,

Li³

et al. 2020

CMAR

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Non-small cell lung cancer (NSCLC) accounts for approximately 80-85% of all lung cancers, with the FAS-associated factor 1 (FAF1) acting as a tumor suppressor. MicroRNAs (miRNAs) can influence cancer progression by targeting oncogenes or antioncogenes. In this study, we aimed to reveal the influence of miR-26a-5p on the regulation of FAF1 expression and NSCLC progression, with the motivation of identifying a potential therapeutic target for NSCLC treatment. Methods: A dual-luciferase reporter assay was used to check for the direct targeting of FAF1 by miR-26a-3p. The miR-26a-5p inhibitor or FAF1 shRNA plasmid was transfected into A549 and H1299 cells to modulate FAF1 expression. Then, the effect of miR-26a-5p/ FAF1 on cellular functions was investigated. MTT assay was used to evaluate cell viability. EdU proliferation assay and cell cycle assay were performed to analyze the effect of miR-26a-5p on cell replication and cell cycle. We used annexin V-FITC and PI to stain apoptotic cells, followed by flow cytometric analysis. Transwell and wound healing assays were performed to investigate metastasis. Moreover, the effect of miR-26a-5p/FAF1 on cancer progression was examined in vivo. Lastly, the underlying mechanism was uncovered using RT-qPCR, Western blotting, and TOP/FOP flash assay. Results: miR-26a-5p was found to directly target FAF1 and downregulate its expression. Blocking miR-26a-5p inhibited the cell growth, migration, and invasion, but promoted cell apoptosis. In addition, this inhibited the growth of tumor in mice. FAF1 knockdown reversed the functions of miR-26a-5p. Further, miR-26a-5p/FAF1 was observed to play an important role in the Wnt signaling pathway, regulating the expression of genes such as AXIN, c-Myc, and cyclin-D1. Conclusion: Taken together, we show that miR-26a-5p functions as an oncogenic microRNA in NSCLC by targeting FAF1 and may serve as a potential target for NSCLC treatment.

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“…9(c), samples with low expression are at greater risk of survival (HR=0.602, 95% CI =0.407 to 0.891). In fact, in previous studies, the two microRNAs have been reported to be tumor suppressor microRNAs that often suppress bladder cancer development by inhibiting expression of some oncogenes [35]- [37]. We also analyzed the GO and KEGG enrichment of mRNAs in MRM 4.…”

Section: E the Prognostic Signatures Of Mrmsmentioning

confidence: 99%

Identification of MicroRNA Regulatory Modules by Clustering MicroRNA-Target Interactions

Yang

Wan

2020

IEEE Access

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Identification of microRNA regulatory modules can help decipher microRNA synergistic regulatory mechanism in the development and progression of complex diseases, especially cancers. Experimentally validated microRNA-target interactions provide strong direct evidence for the analysis of microRNA regulatory functions. We here developed a novel computational framework named CMIN to identify microRNA regulatory modules by performing link clustering on such experimentally verified microRNA-target interactions. CMIN runs in two main steps: it first utilizes convolutional autoencoders to extract high-level microRNA-target interaction features from the expression profile data, and then applied affinity propagation clustering algorithm to interaction feature to obtain overlapping microRNA-target clusters. Clusters with significant synergy correlations are considered as microRNA regulatory modules. We tested the proposed framework and other three existing methods on three types of cancer data sets from TCGA (The Cancer Genome Atlas). The results showed that the microRNA regulatory modules detected by CMIN exhibit stronger topological correlation and more functional enrichment compared with other methods. Availability: The supplementary files of CMIN are available at https://github.com/snryou/CMIN.

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Enhanced plasma miR‑26a‑5p promotes the progression of bladder cancer via targeting PTEN

Cited by 16 publications

References 27 publications

MiR-26a-5p enhances cells proliferation, invasion, and apoptosis resistance of fibroblast-like synoviocytes in rheumatoid arthritis by regulating PTEN/PI3K/AKT pathway

MiR-26a-5p enhances cells proliferation, invasion, and apoptosis resistance of fibroblast-like synoviocytes in rheumatoid arthritis by regulating PTEN/PI3K/AKT pathway

<p>MiR-26a-5p Serves as an Oncogenic MicroRNA in Non-Small Cell Lung Cancer by Targeting FAF1</p>

Identification of MicroRNA Regulatory Modules by Clustering MicroRNA-Target Interactions

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