Astrocyte Elevated Gene-1 Increases Invasiveness of NSCLC Through Up-Regulating MMP7

Zhu, Ren; Tian, Ye

doi:10.1159/000430242

Cited by 13 publications

(10 citation statements)

References 33 publications

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“…In addition, multivariate analysis indicated that MTDH expression is an independent prognostic factor for both overall survival and disease-free survival in NSCLC (29). Functional experiments demonstrated that MTDH is involved in NSCLC progression by playing a role in cell proliferation, apoptosis, motility and epithelial-to-mesenchymal transition (28,30,(52)(53)(54). In our study, we confirmed that miR-584 may inhibit NSCLC progression by directly targeting MTDH and indirectly regulating PTEN/AKT pathway.…”

Section: Discussionsupporting

confidence: 76%

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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: Discussionsupporting

confidence: 76%

“…Among these candidates, MTDH, which was upregulated in NSCLC and involved in NSCLC occurrence and progression (28)(29)(30), was chosen for confirmatory test (Fig. 3A).…”

Section: Mtdh Is a Direct Target Gene Of Mir-584 In Nsclcmentioning

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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“…As an important mechanism of tumor metastasis, EMT has been observed in many different types of cancers, including NSCLC [35-37]. EMT is a conserved cellular process in which epithelial cells temporarily lose their cell polarity and develop characteristics of interstitial cells, which can invade and migrate through the body.…”

Section: Discussionmentioning

confidence: 99%

“…McCarroll has reported that loss of PTEN/AKT activity can promote tumorigenesis in NSCLC, which explains the changes in proliferation and cell cycle between the treated and control cells [41]. Additionally, as a downstream molecule of many regulatory factors, such as miRNA-10a, TOPK/PBK, PUMA and others, PTEN/AKT has been shown to influence the drug resistance and prognosis of NSCLC [37, 42-44]. Furthermore, we reduced the expression of PTEN in FAL1 knockdown cells and found that the effect of FAL1 siRNA interference was partially rescued, which demonstrated our assumption of the presence of a FAL1-PTEN/AKT-EMT regulation pathway.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA FAL1 Promotes Cell Proliferation, Invasion and Epithelial-Mesenchymal Transition Through the PTEN/AKT Signaling Axis in Non-Small Cell Lung Cancer

Pan

Yao

Liu

et al. 2017

Cell Physiol Biochem

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Background/Aims: Recently, long non-coding RNAs (lncRNAs) have been found to have many biological effects in different cancer stages. Several studies have revealed that focally amplified lncRNA on chromosome 1 (FAL1) regulates cancer progression via p21. However, the expression and mechanism of FAL1 in non-small cell lung cancer (NSCLC) still remain unclear. Methods: We detected the FAL1 level in NSCLC tissues and in established cell lines using quantitative real-time PCR and evaluated the clinical significance. FAL1 was silenced or overexpressed using siRNA or lentivirus to study whether FAL1 affected cell proliferation, invasion and migration. Xenograft growth and pulmonary metastasis were observed using nude mouse models. The mechanisms were explored with western blotting and immunohistochemistry. Results: FAL1 was significantly overexpressed in NSCLC compared with adjacent normal tissues, and a high level of FAL1 correlated with poor histological grade, increased lymph node metastasis and advanced TNM stage. Loss- and gain-of-function experiments in vitro verified that knockdown of FAL1 inhibited cell proliferation, invasion, migration and EMT via the PTEN/AKT pathway. Furthermore, an in vivo assay confirmed that overexpression of FAL1 facilitated tumor growth and metastasis. Conclusion: FAL1 may promote tumorigenesis and progression of NSCLC through the PTEN/AKT axis, which could lead to lncRNA-related diagnostics and therapeutics in NSCLC.

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“…Metastasis is a complex process that contributes to the most common cause of mortality in NSCLC patients. During metastasis, a series of molecular and cellular events occur, including degradation of base membrane, cell migration and invasion and cell adhesion at new location [29]. It is important to note that, it is possible that MSI1 also functions in other processes that facilitated metastasis of NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

Musashi1 Promotes Non-Small Cell Lung Carcinoma Malignancy and Chemoresistance via Activating the Akt Signaling Pathway

Lang

Kong

et al. 2017

Cell Physiol Biochem

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Background/Aims: Lung cancer is one of the leading causes for cancer mortality. The poor therapeutic outcome of non-small cell lung carcinoma (NSCLC) is mainly due to late diagnosis and chemoresistance. In this study, we investigated the role of Musashi1 (MSI1) in NSCLC malignancy and chemoresistance. Methods: Colony formation, MTT, glucose uptake and lactate production assays were employed to study lung cancer cell malignancy and chemoresistance. RT-PCR and Western blotting were performed to detect mRNA and protein expressions of genes. We used immunohistochemistry and Pearson correlation analysis to study the relationship of gene expression. Results: We demonstrated that MSI1 was able to promote the proliferation and glucose metabolism of NSCLC cells, and to mediate the sensitivity to chemotherapy drugs in NSCLC cells. Importantly, we found that MSI1 could regulate the activity of Akt signaling. The regulation of NSCLC proliferation, glucose metabolism and chemoresistance by MSI1 was dependent on the modulation of the activity of the Akt signaling pathway. We also found that MSI1 was a target of miR-181a-5p, a microRNA involved in the regulation of cancer development. The expression levels of MSI1 and miR-181a-5p were negatively correlated in NSCLC. Conclusion: MSI1 promotes non-small cell lung carcinoma malignancy and chemoresistance via activating the Akt signaling pathway, which provides a new strategy for the therapy of NSCLC.

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Astrocyte Elevated Gene-1 Increases Invasiveness of NSCLC Through Up-Regulating MMP7

Cited by 13 publications

References 33 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

Long Noncoding RNA FAL1 Promotes Cell Proliferation, Invasion and Epithelial-Mesenchymal Transition Through the PTEN/AKT Signaling Axis in Non-Small Cell Lung Cancer

Musashi1 Promotes Non-Small Cell Lung Carcinoma Malignancy and Chemoresistance via Activating the Akt Signaling Pathway

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