miR-30 overexpression promotes glioma stem cells by regulating Jak/STAT3 signaling pathway

Che, Shusheng; Sun, Tingting; Wang, Jianpeng; Jiao, Yingbin; Wang, Chao; Meng, Qingcai; Qi, Weiguo; Zhang, Yan

doi:10.1007/s13277-015-3400-8

Cited by 39 publications

(36 citation statements)

References 21 publications

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“…Zhao et al [26] found that miR-30a functions as a tumor suppressor by targeting the oncogenic Wnt/beta-catenin/BCL9 pathway in H929 cells. Che et al [27] found that miR-30 overexpression promoted glioma stem cells by regulating the Jak/STAT3 signaling pathway. miR-30a activity was also found to be regulated by competitive endogenous RNA (ceRNA).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting <italic>EYA2</italic>

Yao¹,

Zheng²,

Li³

et al. 2016

ABBS

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MicroRNAs (miRNAs) are a class of small non-coding RNAs and closely related to the pathogenesis of cancers. Increasing evidence indicates that miR-30a plays a profound role during the development of cancers. However, the functions of miR-30a in non-small-cell lung cancer (NSCLC) are still ambiguous. Here we found that miR-30a was decreased in lung adenocarcinoma A549 cells and in tissue samples from 14 patients by qRT-PCR, and also found that overexpression of miR-30a in A549 cells inhibited migration and invasion but not cell proliferation and cell cycle progression by wound-healing assay, matrigel invasion assay, MTS-based cell proliferation assay, and flow cytometry-based cell cycle analysis, respectively. We further explored the potential mechanism of miR-30a-mediated gene regulation in lung adenocarcinoma cell lines. EYA2 is a predicted target of miR-30a, and it has been found that EYA2 expression is inhibited by miR-30a in breast cancer cells. We demonstrated that EYA2 is a direct target of miR-30a by using the dual-luciferase reporter assay in A549 cells and showed that EYA2 protein levels are inversely correlated with miR-30a expression in A549 and BEAS-2B cells. In addition, we also confirmed the rescue effects of EYA2 overexpression in A549 cells by cotransfection with EYA2 expression vector and miR-30a mimics. Taken together, our results demonstrate that overexpression of miR-30a in lung adenocarcinoma A549 cells can inhibit cell migration and invasion, which is partially attributed to the decrease of EYA2 expression. Our findings suggest that miR-30a may be used as a new potential target for the treatment of lung adenocarcinoma in the future.

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Section: Discussionmentioning

confidence: 99%

Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting <italic>EYA2</italic>

Yao¹,

Zheng²,

Li³

et al. 2016

ABBS

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“…322 MiR-30 targets SOCS3 in glioma stem cells. 337 Mir-93 downregulates the expression of JAK1 and STAT3 to induce the differentiation of breast CSCs. Mir-218 negatively regulates the IL-6 receptor and JAK3 gene expression in lung CSCs.…”

Section: Major Signaling Pathways In Cscsmentioning

confidence: 99%

Targeting cancer stem cell pathways for cancer therapy

Yang

Shi

Zhao

et al. 2020

Sig Transduct Target Ther

1,261

998

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Since cancer stem cells (CSCs) were first identified in leukemia in 1994, they have been considered promising therapeutic targets for cancer therapy. These cells have self-renewal capacity and differentiation potential and contribute to multiple tumor malignancies, such as recurrence, metastasis, heterogeneity, multidrug resistance, and radiation resistance. The biological activities of CSCs are regulated by several pluripotent transcription factors, such as OCT4, Sox2, Nanog, KLF4, and MYC. In addition, many intracellular signaling pathways, such as Wnt, NF-κB (nuclear factor-κB), Notch, Hedgehog, JAK-STAT (Janus kinase/signal transducers and activators of transcription), PI3K/AKT/mTOR (phosphoinositide 3-kinase/AKT/mammalian target of rapamycin), TGF (transforming growth factor)/SMAD, and PPAR (peroxisome proliferator-activated receptor), as well as extracellular factors, such as vascular niches, hypoxia, tumor-associated macrophages, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, extracellular matrix, and exosomes, have been shown to be very important regulators of CSCs. Molecules, vaccines, antibodies, and CAR-T (chimeric antigen receptor T cell) cells have been developed to specifically target CSCs, and some of these factors are already undergoing clinical trials. This review summarizes the characterization and identification of CSCs, depicts major factors and pathways that regulate CSC development, and discusses potential targeted therapy for CSCs.Signal Transduction and Targeted Therapy (2020) 5:8; https://doi.

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“…Previous studies have highlighted the importance of miR-30 in the development and progression of cancer (20)(21)(22)(23). It has previously been demonstrated that miR-30 is associated with inflammatory responses (24-26).…”

Section: Discussionmentioning

confidence: 99%

Immune regulation of miR-30 on the Mycobacterium tuberculosis-induced TLR/MyD88 signaling pathway in THP-1 cells

Sun

Dai

2017

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to examine the expression of microRNA (miR)-30 family members in THP-1 human monocytes cells during Mycobacterium tuberculosis (MTB) H37Rv infection, and to investigate the role of miR-30 in the regulation of MTB-induced Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) activation and cytokine expression. The THP-1 cells were infected with MTB H37Rv and the expression of miR-30 family members was determined by reverse transcription-quantitative polymerase chain reaction analysis. In addition, miR-30a and miR-30e mimics were transfected into THP-1 cells to overexpress miR-30a and miR-30e. The expression of TLR2, TLR4 and MyD88 was determined by western blot analysis, and the expression of the cytokines tumor necrosis factor-α, interleukin (IL)-6, and IL-8 was determined using ELISA assays. A luciferase reporter assay was used to identify the target gene of miR-30a. MTB infection was demonstrated to significantly induce miR-30a and miR-30e expression in THP-1 cells in a time-dependent manner. Forced overexpression of miR-30a, but not miR-30e, exhibited an inhibitory effect on TLR/MyD88 activation and cytokine expression in the uninfected and MTB-infected THP-1 cells. The luciferase reporter assay demonstrated that miR-30a directly regulates the transcriptional activity of the MyD88 3'-untranslated region. In conclusion, the present study, to the best of our knowledge, is the first to demonstrate that miR-30a suppresses TLR/MyD88 activation and cytokine expression in THP-1 cells during MTB H37Rv infection, and that MyD88 is a direct target of miR-30a. The current study may aid in the development of novel therapeutic approaches for treating MTB.

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miR-30 overexpression promotes glioma stem cells by regulating Jak/STAT3 signaling pathway

Cited by 39 publications

References 21 publications

Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting <italic>EYA2</italic>

Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting <italic>EYA2</italic>

Targeting cancer stem cell pathways for cancer therapy

Immune regulation of miR-30 on the Mycobacterium tuberculosis-induced TLR/MyD88 signaling pathway in THP-1 cells

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miR-30 overexpression promotes glioma stem cells by regulating Jak/STAT3 signaling pathway

Cited by 39 publications

References 21 publications

Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting &lt;italic&gt;EYA2&lt;/italic&gt;

Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting &lt;italic&gt;EYA2&lt;/italic&gt;

Targeting cancer stem cell pathways for cancer therapy

Immune regulation of miR-30 on the Mycobacterium tuberculosis-induced TLR/MyD88 signaling pathway in THP-1 cells

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Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting <italic>EYA2</italic>

Overexpression of miR-30a in lung adenocarcinoma A549 cell line inhibits migration and invasion via targeting <italic>EYA2</italic>