MiR-486-5p inhibits IL-22-induced epithelial-mesenchymal transition of breast cancer cell by repressing Dock1

Liu, Hongli; Mou, Qingjie; Li, Peirui; Yang, Zhiyi; Wang, Zhaoyan; Niu, Jie; Liu, Yuanyuan; Sun, Zhi-Liang; Lv, Shijun; Zhang, Baogang; Chen, Yin

doi:10.7150/jca.30596

Cited by 38 publications

(38 citation statements)

References 34 publications

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“…The malignant progression of NSCLC is considered to be a comprehensive event that includes a gene expression network and alterations in the tumor microenvironment, in which microRNAs play critical roles [39]. MiR-486-5p, widely documented to be a tumor-suppressive microRNA, inhibits proliferation and invasion in many types of cancers [39,40], In the present study, we observed an interaction between EVI5 and miR-486-5p. To address this question, a dualluciferase reporter assay was performed, and it showed that miR-486-5p significantly inhibited luciferase activity in cells transfected with the wild-type EVI5 3′-UTR, Moreover, overexpression of miR-486-5p prevented EVI5-induced cell proliferation, migration and invasion in NSCLC cells, which further confirms the tumorpromoting function of EVI5 and provides more clues to the regulation network of EVI5.…”

Section: Discussionsupporting

confidence: 60%

EVI5 is an oncogene that regulates the proliferation and metastasis of NSCLC cells

Cai

Zhou

Zeng

et al. 2020

J Exp Clin Cancer Res

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Background: The Ecotropic viral integration site 5 (EVI5), an important protein in regulating cell cycle, cytokinesis and cellular membrane traffic, functions as a stabilizing factor maintaining anaphase-promoting complex/cyclosome (APC/C) inhibitor Emi1 in S/G2 phase. However, the mechanism by which EVI5 promotes malignant transformation of non-small cell lung cancer (NSCLC) remains unknown. In the present study, we addressed the role of EVI5 in NSCLC by regulating tumor growth, migration and invasion. Methods: The expression levels of EVI5 and miR-486-5p in NSCLC tissues and cells were measured by real-time PCR. Meanwhile, EVI5 and its associated protein expression were analyzed by western blot and coimmunoprecipitation assay. Flow cytometry was performed to determine cell proliferation and apoptosis. CCK-8 and clonogenic assays were used to analyze cell viability. Wound healing, transwell migration and matrigel invasion assays were utilized to assess the motility of tumor cells. To investigate the role of EVI5 in vivo, lung carcinoma xenograft mouse model was applied.. Results: EVI5 was upregulated in NSCLC tissues and cell lines when compared with that in normal tissues and cell line. Knockdown of EVI5 in vitro inhibited tumor cell proliferation, migration and invasion in NSCLC cells. Further, inoculation of EVI5-deficient tumor cells into nude mice suppressed tumor proliferation and metastasis compared to control mice inoculated with unmanipulated tumor cells. These data indicated that EVI5 promote the proliferation of NSCLC cells which was consistent with our previous results. Additionally, we showed that EVI5 was directly regulated by miR-486-5p, and miR-486-5p-EVI5 axis affected the NSCLC migration and invasion through TGF-β/Smad signaling pathway by interacting with TGF-β receptor II and TGF-β receptor I. Conclusions: Based on these results, we demonstrated a new post-transcriptional mechanism of EVI5 regulation via miR-486-5p and the protumoral function of EVI5 in NSCLC by interacting with Emi1 and/or TGF-β receptors, which provides a new insight into the targeted therapy of NSCLC.

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Section: Discussionsupporting

confidence: 60%

EVI5 is an oncogene that regulates the proliferation and metastasis of NSCLC cells

Cai

Zhou

Zeng

et al. 2020

J Exp Clin Cancer Res

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“…Previous researches have unmasked that miR‐486‐5p elicits a repressive effect on tumor progression. For example, miR‐486‐5p represses Dock1 and inhibits IL‐22‐induced EMT processes 26 . MiR‐486‐5p suppresses non‐small cell lung cancer progression 27 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00857 regulates the progression and glycolysis in ovarian cancer by modulating the Hippo signaling pathway

Lin

Feng

et al. 2020

Cancer Medicine

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Ovarian cancer is one of the most common gynecological cancers with high morbidity and mortality, which seriously endangers women's health and quality of life. Long noncoding RNAs (lncRNAs) can regulate the progression of cancers, including ovarian cancer. LINC00857 (long intergenic non‐protein coding RNA 857) has been discovered to be a crucial factor in the regulation of cancer development. Nevertheless, the specific functions and mechanisms of LINC00857 in ovarian cancer remain unclear. The Hippo signaling pathway can involve in cancer progression. In our research, we aimed to investigate the correlation of LINC00857 and Hippo pathway. Quantitative real‐time polymerase chain reaction assay was utilized to test the expression of LINC00857 in ovarian cancer tissues and cells. Functional experiments revealed that LINC00857 silencing led to the inhibition on cell proliferation, migration, invasion, and glycolysis but accelerated cell apoptosis in ovarian cancer. Mechanism experiments, including RNA immunoprecipitation, RNA pull‐down, and luciferase reporter experiments demonstrated that LINC00857 could regulate YAP1 (Yes1 associated transcriptional regulator) by competitively binding to miR‐486‐5p in ovarian cancer. In a word, this study unveiled that LINC00857 regulates YAP1 by competitively binding to miR‐486‐5p and accelerates ovarian cancer progression.

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“…By regulating SLC2A1/GLUT1, miR-328 participates in the Warburg effect in COAD (Santasusagna et al, 2018). MiR-486 is related to the molecular mechanisms of several cancers, including cervical cancer (Li et al, 2018a), breast cancer (Li et al, 2019), lung cancer (Tian et al, 2019), esophageal cancer (Lang and Zhao, 2018), ovarian cancer (Ma et al, 2016), and pancreatic cancer (Xia et al, 2019). Kelley et al nearly demonstrated that the expression of miR-486 associates with early-stage of COAD (Kelley et al, 2018).…”

Section: Identification Of Mirna With Prognostic Value In Coadmentioning

confidence: 99%

MicroRNAs Associated With Colon Cancer: New Potential Prognostic Markers and Targets for Therapy

Zhu

Xü

Liu

et al. 2020

Front. Bioeng. Biotechnol.

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MicroRNAs (miRNAs) are a kind of non-coding RNA (ncRNA) that regulate the expression of target genes and play a role in the occurrence and development of cancers. Colon cancer (COAD) is the second most common cause of cancer-related mortality. However, the prognostic value of miRNAs in COAD is still confusing. In this study, we obtain miRNAs and messenger RNAs (mRNAs) expression profiles of COAD from the Cancer Genome Atlas (TCGA) database. After preliminary data screening and preprocessing, we acquire the expression data of 894 miRNAs and 17,019 mRNAs. Then, compared with the normal samples, 39 upregulated miRNAs and 54 downregulated miRNAs are identified by differential expression analysis. Furthermore, we obtain 1,487 upregulated mRNAs and 2,847 downregulated mRNAs. We confirm nine key miRNAs related to the survival rate of COAD patients. Moreover, by using bioinformatics methods, we get 461 common genes from both the target genes of these nine key miRNAs and differentially expressed mRNAs. Through analyzing the protein-protein interaction (PPI) network of these 461 common genes and survival analysis, we confirm five hub genes as promising biomarkers for COAD prognosis. It is worth mentioning that no previous reports have found that PGR and KCNB1 are related to COAD. We expect these key miRNAs and hub genes will provide a new way for the study of COAD.

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MiR-486-5p inhibits IL-22-induced epithelial-mesenchymal transition of breast cancer cell by repressing Dock1

Cited by 38 publications

References 34 publications

EVI5 is an oncogene that regulates the proliferation and metastasis of NSCLC cells

EVI5 is an oncogene that regulates the proliferation and metastasis of NSCLC cells

LncRNA LINC00857 regulates the progression and glycolysis in ovarian cancer by modulating the Hippo signaling pathway

MicroRNAs Associated With Colon Cancer: New Potential Prognostic Markers and Targets for Therapy

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