MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Li, Xizhe; Zhu, Jiali; Liu, Yuanqi; Duan, Chaojun; Chang, Ruimin; Zhang, Chunfang

doi:10.1111/cas.14014

Cited by 51 publications

(53 citation statements)

References 41 publications

(70 reference statements)

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“…Therefore, further investigation of the cancer-associated miRNAs that are crucial for the pathogenesis of NSCLC may provide effective therapeutic targets for patients with this aggressive malignant tumor. Recently, the functions of miRNAs in the progression and development of NSCLC have been gradually recognized (42)(43)(44). The present study demonstrated that miR-877 may exhibit tumor suppressor action in NSCLC by directly targeting IGF-1R.…”

Section: Discussionsupporting

confidence: 49%

MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

et al. 2019

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MicroRNAs (miRNAs/miRs) are frequently differentially expressed in non-small cell lung cancer (NSCLC), and differential miRNAs expression may be closely associated with NSCLC genesis and development. Therefore, an in-depth investigation of the cancer-associated miRNAs that are crucial for NSCLC pathogenesis may provide effective therapeutic targets for patients with this aggressive malignant tumor type. The expression levels and roles of miR-877 have been well studied in hepatocellular carcinoma and renal cell carcinoma. However, the expression pattern and functions of miR-877 in NSCLC as well as associated underlying mechanisms, to the best of our knowledge, have not yet been investigated. The present study revealed that miR-877 expression was downregulated in NSCLC tissues and cell lines. Low miR-877 expression was significantly associated with TNM stage and distant metastasis in patients with NSCLC. Functional experiments demonstrated that recovery of miR-877 expression restricted the proliferation and invasion of NSCLC cells. In addition, bioinformatics analysis predicted insulin-like growth factor 1 receptor (IGF-1R) as a potential target of miR-877. Luciferase reporter assays, reverse transcription-quantitative PCR and western blot analysis further validated that IGF-1R was a direct target of miR-877 in NSCLC. Furthermore, IGF-1R expression was markedly upregulated in NSCLC tissues, and exhibited an inverse correlation with miR-877 expression. Additionally, IGF-1R overexpression reversed the inhibitory effects in NSCLC cells caused by miR-877 upregulation. These findings demonstrated that miR-877 attenuated NSCLC cell proliferation and invasion, at least partly, by downregulating IGF-1R expression, thereby providing an new candidate biomarker for the diagnosis and therapy of patients with NSCLC.

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Section: Discussionsupporting

confidence: 49%

MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

et al. 2019

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“…29 In breast cancer, ERBB2 is negatively regulated by miR-155, promoting the malignant transformation of breast epithelial cells; 13 in non-small-cell lung cancer, miR-331-3p inhibits epithelial-mesenchymal transition partly by targeting ERBB2. 30 In this study, ERBB2 was identified as a target gene of miR-193a-5p and could be negatively regulated by it. Previous studies and our findings imply that the dysregulation of miRNAs could be an important reason for ERBB2 activation in cancers.…”

Section: Discussionmentioning

confidence: 79%

<p>Long Non-Coding RNA Cancer Susceptibility 9 (CASC9) Up-Regulates the Expression of ERBB2 by Inhibiting miR-193a-5p in Colorectal Cancer</p>

Ding

Zhang

et al. 2020

CMAR

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Background: Emerging studies have reported that long non-coding RNAs (lncRNAs) were crucial regulators in the progression of colorectal cancer (CRC). LncRNA susceptibility 9 (CASC9) was involved in several cancers; however, its role in CRC remains unknown. Methods: RT-PCR was done to probe the expression of CASC9 and miR-193a-5p in CRC samples. CRC cell lines (HCT116 and SW480) were used as cell models. The biological influence of CASC9 on cancer cells was studied using CCK-8 assay, Transwell assay and TUNEL assay in vitro, and subcutaneous xenotransplanted tumor model in vivo. Interaction between CASC9 and miR-193a-5p was investigated by bioinformatics analysis, RT-PCR, and luciferase reporter assay. The expression level of the downstream gene of miR-193a-5p, erb-b2 receptor tyrosine kinase 2 (ERBB2), was tested by Western blot. Results: CASC9 was significantly up-regulated in CRC samples, while miR-193a-5p was markedly down-regulated. Overexpression of CASC9 promoted viability, migration and invasion of CRC cells, while overexpression of miR-193a-5p had the opposite effect. CASC9 could down-regulate miR-193a-5p via sponging it, and there was a negative relevancy between CASC9 and miR-193a-5p in CRC samples. CASC9 also enhanced the expression levels of ERBB2, while this effect could be reversed by co-transfection with miR-193a-5p. Conclusion: CASC9, an oncogenic lncRNA, was abnormally up-regulated in CRC tissues, and it could indirectly modulate the expression of ERBB2 via reducing the expression level of miR-193a-5p.

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“…miR-331-3p, located on 12q22n and a member of the miR-331 family, functions as a tumor suppressor in CRC; marked downregulation of miR-331-3p in CRC is linked to increased cell proliferation and decreased apoptosis (12,13). This aberrant expression of miR-331-3p is also linked to cell proliferation and migration in various other cancers, such as acute lymphocytic leukemia, lung cancer, glioblastoma, gastric cancer, prostate cancer, non-small cell lung cancer and pancreatic cancer (14)(15)(16)(17)(18)(19)(20). The functions of miR-331-3p in CRC cell migration, as well as the up-and downstream regulatory mechanisms of miR-331-3p, are unclear.…”

Section: Introductionmentioning

confidence: 99%

Hsa_circ_0038646 promotes cell proliferation and migration in colorectal cancer via miR‑331‑3p/GRIK3

Zhou

Chen

et al. 2020

Oncol Lett

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Increasing evidence supports the essential roles of circular RNAs (circRNAs) and microRNAs (miRNAs/miRs) in different types of human cancer. For example, hsa_ circ_0137008 functions as a sponge for mi-338-5p and inhibits the malignant phenotype in colorectal cancer. Furthermore, hsa_circ_RNA_0011780 downregulates FBXW7 by targeting miR-554a and suppressing the progression of non-small cell lung cancer. Thus far, only a single report has identified that the miRNA miR-331-3p exerts a pivotal effect on human colorectal cancer (CRC) evolution. However, both the upand downstream regulatory mechanisms of miR-331-3p are unclear. In the present study, it was predicted via bioinformatics analysis that the circRNA, hsa_circ_0038646, and the glutamate receptor ionotropic kainate 3 (GRIK3) gene contain binding sites that can interact with miR-331-3p. Thus, hsa_ circ_0038646/miR-331-3p/GRIK3 may be a novel therapeutic pathway for CRC. Reverse transcription-quantitative PCR and western blotting analyses were performed, as well as cell proliferation, luciferase reporter and Transwell migration assays. Hsa_circ_0038646 was overexpressed in both CRC cells and tissues, and this aberrant expression was positively related with increasing tumor grade. Knockdown of hsa_circ_0038646 significantly weakened human CRC cell proliferation and migration. It was shown that hsa_circ_0038646 can sponge miR-331-3p to suppress its expression, and that suppression of miR-331-3p can reverse the effects of hsa_circ_0038646 inhibition in CRC cells. It was determined that GRIK3 is a downstream target of miR-331-3p, and that hsa_circ_0038646 could increase the levels of GRIK3 by suppressing miR-331-3p in CRC cells. Restoring GRIK3 expression rescued the weakened CRC cell proliferation and migration following hsa_circ_0038646 knockdown. The present study indicated that hsa_circ_0038646 functions as a tumor promoter in CRC by increasing GRIK3 expression via sponging of miR-331-3p. The hsa_circ_0038646/miR-331-3p/GRIK3 axis may be a novel therapeutic and diagnostic target of CRC.

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MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Cited by 51 publications

References 41 publications

MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

MicroRNA‑877 inhibits cell proliferation and invasion in non‑small cell lung cancer by directly targeting IGF‑1R

<p>Long Non-Coding RNA Cancer Susceptibility 9 (CASC9) Up-Regulates the Expression of ERBB2 by Inhibiting miR-193a-5p in Colorectal Cancer</p>

Hsa_circ_0038646 promotes cell proliferation and migration in colorectal cancer via miR‑331‑3p/GRIK3

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