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 36 publications

(33 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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“…Total proteins were extracted from breast cancer cell lines as previously stated. 17 The following antibodies were used in this study: β-actin (1:5000), vimentin (1:500), Ecadherin (1:500), fibronectin 1 (FN1) (1:500), β-catenin (1:500), c-Myc (1:500), c-Jun (1:500), LEF1 (1:500), MMP2 (1:500). β-actin was used for normalization.…”

Section: Western Blot and Immunofluorescencementioning

confidence: 99%

MiR‐429 suppresses proliferation and invasion of breast cancer via inhibiting the Wnt/β‐catenin signaling pathway

Zhang

Liu

et al. 2020

Thoracic Cancer

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Background microRNAs ( miRNAs) have been verified as molecular targets for regulating tumor proliferation, invasion, and metastasis in tumor progression. However, the relationship between miRNAs and cellular energy metabolism in breast cancer still needs to be clarified. This study aimed to investigate the role of miR‐429 in breast cancer progression. Methods Bioinformatic analyses were employed to detect the relationship between miR‐429 and cancer‐related signaling pathways. We used a Kaplan‐Meier curve to analyze survival rate in patients with high or low expression of miR‐429. We used real‐time quantitative PCR (RT‐qPCR) to detect the expression of miR‐429 in different cell lines. Sh‐con, over‐miR‐429, miR‐429 inhibitor, and sh‐inhibitor control were transfected. Colony formation and EDU assay were used to detect the proliferation of transfected cells. Wound healing and transwell assays were performed to detect the mobility and invasion ability of transfected cells. Western blot assay was used to detect relative protein expression in transfected cells and different tissues. Bioinformatic analyses were conducted to detect the target proteins expression in different breast cancer databases. Dual luciferase reporter assay was used to confirm the binding site between miR‐429 and fibronectin 1 (FN1). Results The results of our study indicate that MiR‐429 and its target genes are associated with cancer‐related signaling pathways and that higher miR‐429 expression corresponds with a better prognosis. When miR‐429 was overexpressed, the proliferation, invasion of MDA‐MB‐231 were inhibited. MiR‐429 was able to suppress the Wnt/β‐catenin signaling pathway, and FN1 overexpression could rescue the influence of over‐miR‐429. Conclusions The results of our study suggest that miR‐429 suppresses the proliferation and invasion of breast cancer via inhibiting the Wnt/β‐catenin signaling pathway.

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

Cited by 36 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

MiR‐429 suppresses proliferation and invasion of breast cancer via inhibiting the Wnt/β‐catenin signaling pathway

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