MicroRNA-320a is downregulated in non-small cell lung cancer and suppresses tumor cell growth and invasion by directly targeting insulin-like growth factor 1 receptor

Wang, Jianguo; Shi, Chunyun; Wang, Jianfei; Cao, Li; Zhong, Li; Wang, Dongmei

doi:10.3892/ol.2017.5863

Cited by 32 publications

(22 citation statements)

References 35 publications

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“…Multiple risk factors of lung cancer have been validated, such as environmental deterioration, tobacco use and exposure to radon and occupational carcinogens (2)(3)(4)(5). Non-small cell lung cancer (NSCLC), which accounts for approximately 80% of the total lung cancer cases, is classified into three subtypes: Squamous cell carcinoma, adenocarcinoma, and large cell carcinoma (6). The current therapeutic treatments used in NSCLC patients include surgery resection, chemotherapy and radiotherapy, and these strategies can be applied alone or in combination depending on the extent and progression of the disease (7).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-584 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting MTDH

Zhang

Wang

2017

Exp Ther Med

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Abstract. Lung cancer is the third most frequent human malignant tumour and the leading cause of cancer-associated mortality worldwide. Emerging lines of evidence have demonstrated that microRNAs (miRNAs) are upregulated or downregulated in non-small cell lung cancer (NSCLC), and this phenomenon is involved in the regulation of various processes during tumorigenesis and progression, including tumour groWTh, apoptosis, cell invasion, and tumour metastasis. Therefore, understanding the molecular mechanism that associates abnormally expressed miRNAs with NSCLC formation and development may lead to the identification of novel diagnostic, and therapeutic targets for patients with NSCLC. miRNA-584 (miR-584) functions as a tumour suppressor in several types of cancer. However, the expression pattern, detailed biological function and underlying molecular mechanism of miR-584 in NSCLC remain unclear. Therefore, the present study detected the expression of miR-584 in NSCLC, investigated its role in NSCLC cells and determined its underlying molecular mechanism. In the current study, it was demonstrated that miR-584 was downregulated in NSCLC tissues and cell lines. Low miR-584 expression was correlated with tumour size, tumour node metastasis stage and distant metastasis. Overexpression of miR-584 inhibited cell proliferation and invasion in NSCLC. Additionally, metadherin was identified as a direct target gene of miR-584 in NSCLC as confirmed by a series of experiments. Moreover, upregulation of miR-584 was involved in the regulation of the phosphatase and tensin homolog/Akt serine/threonine kinase signalling pathway in NSCLC. Thus, miR-584 may serve as a tumor-suppressor, and the results of the present study provide a reference for future research into the potential mechanisms underlying NSCLC progression.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-584 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting MTDH

Zhang

Wang

2017

Exp Ther Med

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“…Mir‐320a is de‐regulated in several cancer types such as gastric, breast, colon and lung cancer . Recent works demonstrated the role of mir‐320a as tumor suppressor in NSCLC by directly regulating IGF‐1R or VDAC1 expression suggesting this miRNA as a potential therapeutic target. Furthermore, mir‐320a was also involved in lung metastasis formation through down‐regulation of STAT3 and NRP‐1 .…”

Section: Discussionmentioning

confidence: 99%

Circulating mir‐320a promotes immunosuppressive macrophages M2 phenotype associated with lung cancer risk

Fortunato

Borzi

Milione

et al. 2019

Intl Journal of Cancer

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miRNAs play a central role in the complex signaling network of cancer cells with the tumor microenvironment. Little is known on the origin of circulating miRNAs and their relationship with the tumor microenvironment in lung cancer. Here, we focused on the cellular source and relative contribution of different cell types to circulating miRNAs composing our risk classifier of lung cancer using in vitro/in vivo models and clinical samples. A cell‐type specific expression pattern and topography of several miRNAs such as mir‐145 in fibroblasts, mir‐126 in endothelial cells, mir‐133a in skeletal muscle cells was observed in normal and lung cancer tissues. Granulocytes and platelets are the major contributors of miRNAs release in blood. miRNAs modulation observed in plasma of lung cancer subjects was consistent with de‐regulation of the same miRNAs observed during immunosuppressive conversion of immune cells. In particular, activated neutrophils showed a miRNA profile mirroring that observed in plasma of lung cancer subjects. Interestingly mir‐320a secreted by neutrophils of high‐risk heavy‐smokers promoted an M2‐like protumorigenic phenotype through downregulation of STAT4 when shuttled into macrophages. These findings suggest a multifactorial and nonepithelial cell‐autonomous origin of circulating miRNAs associated with risk of lung cancer and that circulating miRNAs may act in paracrine signaling with causative role in lung carcinogenesis and immunosuppression.

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“…The possible upstream miRNAs that target p100 were predicted using the Targetscan program (http://www.targetscan.org/vert_70). Among the searched items, miR‐320a attracted our attention because p100 3′‐UTR contains a putative target sequence for miR‐320a (Fig a), and several significant reports have found that miR‐320a effectively suppresses lung cancer cell growth and metastasis . We used the dual‐luciferase reporter system to validate miR‐320a targeting of p100 in lung cancer cells.…”

Section: Resultsmentioning

confidence: 99%

“…Among the searched items, miR-320a attracted our attention because p100 3 0 -UTR contains a putative target sequence for miR-320a (Fig 3a), and several significant reports have found that miR-320a effectively suppresses lung cancer cell growth and metastasis. [18][19][20] We used the dual-luciferase reporter system to validate miR-320a targeting of p100 in lung cancer cells. Overexpression of the miR-320a mimics obviously repressed the firefly luciferase reporter activity of the wild-type p100 3 0 -UTR, but did not impact activity of the mutant 3 0 -UTR constructs (Fig 3b), indicating that miR-320a directly targeted p100 by binding to its 3 0 -UTR.…”

Section: Tumor Suppressing Mir-320a Directly Targets P100mentioning

confidence: 99%

p100 functions as a metastasis activator and is targeted by tumor suppressing microRNA‐320a in lung cancer

Xing¹,

Li²,

Gao³

2017

Thoracic Cancer

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BackgroundLung cancer is among the most frequently diagnosed types of cancer worldwide, with high morbidity and mortality. Metastasis accounts for the deadliest and most poorly understood feature of lung cancer. Herein, we demonstrate that SND1 (also known as p100) acts as a candidate metastasis activator and is targeted by microRNA‐320a (miR‐320a) in lung cancer cells.Methodsp100 expression in lung cancer cell lines and tissues was determined by quantitative real time‐PCR and Western blot. RNA interference was applied to investigate the functions of p100 in lung cancer cell migration, reflected by wound healing and transwell assays. Luciferase reporter assay, quantitative real time‐PCR, and Western blot were finally used to examine miR‐320a targeting of p100 in lung cancer cells.Resultsp100 expression was significantly higher in lung cancer cell lines and tissues compared to normal human bronchial epithelial cells and matched normal lung tissues. Downregulation of p100 by RNA interference obviously inhibited lung cancer cell migration in vitro. Moreover, we validated p100 as a direct target of miR‐320a, a tumor suppressing microRNA repressing lung cancer cell migration. Finally, we showed an inversely expressed correlation between p100 and miR‐320a in tested lung cancer tissues and cell lines, both of which acted as important prognostic factors in lung cancer.ConclusionOur findings identify that p100, targeted by tumor suppressing miR‐320a, is a key metastasis activator in lung cancer, and both p100 and miR‐320a could be considered as biomarkers for prognosis of lung cancer patients.

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MicroRNA-320a is downregulated in non-small cell lung cancer and suppresses tumor cell growth and invasion by directly targeting insulin-like growth factor 1 receptor

Cited by 32 publications

References 35 publications

MicroRNA-584 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting MTDH

MicroRNA-584 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting MTDH

Circulating mir‐320a promotes immunosuppressive macrophages M2 phenotype associated with lung cancer risk

p100 functions as a metastasis activator and is targeted by tumor suppressing microRNA‐320a in lung cancer

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