Knockdown of astrocyte elevated gene-1 inhibited cell growth and induced apoptosis and suppressed invasion in ovarian cancer cells

Wang, Jiewen; Chen, Xiao; Tong, Mengmeng

doi:10.1016/j.gene.2017.03.024

Cited by 16 publications

(8 citation statements)

References 52 publications

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“…AEG-1 downregulation resulted in the inhibition of cell viability and invasive ability and the enhancement of apoptosis. A recent study revealed that knockdown of AEG-1 suppressed cell growth and induced apoptosis and blocked invasion in ovarian cancer cells, 31 which was consistent with our findings. Moreover, AEG-1 was verified to be a target of let-7d .…”

Section: Discussionsupporting

confidence: 92%

<em>let-7d</em> suppresses proliferation and invasion and promotes apoptosis of meningioma by targeting AEG-1

Zhao

2017

OTT

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Backgroundlet-7d has been indicated to act as a tumor suppressor in various cancers. However, the function and molecular mechanism of let-7d in meningioma progression have not been elucidated.Materials and methodsQuantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression levels of let-7d and AEG-1 mRNA in meningioma tissues and cell lines. The protein level of AEG-1 was measured by Western blot analysis. MTT assay, Transwell invasion assay and flow cytometry analysis were carried out to determine the proliferation, invasion and apoptosis of IOMM-Lee and CH-157MN cells, respectively. Target gene of let-7d was verified by luciferase reporter analysis.Resultslet-7d expression was downregulated, and AEG-1 expression was upregulated in meningioma tumor tissues. let-7d overexpression suppressed proliferation and invasion and induced apoptosis in IOMM-Lee and CH-157MN cells. Moreover, AEG-1 was a direct target of let-7d. Restoration of AEG-1 expression reversed let-7d-mediated suppression of the proliferation and invasion and let-7d-induced apoptosis in IOMM-Lee and CH-157MN cells.Conclusionlet-7d repressed proliferation and invasion and promoted apoptosis of meningioma cells by targeting AEG-1. The present study provided a better understanding of the meningioma pathogenesis and a promising therapeutic target for meningioma patients.

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Section: Discussionsupporting

confidence: 92%

<em>let-7d</em> suppresses proliferation and invasion and promotes apoptosis of meningioma by targeting AEG-1

Zhao

2017

OTT

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“…MTDH is a multifunctional oncogene and overexpressed in multiple types of human cancer, including glioma (42), breast cancer (43), gastric cancer (44), colorectal cancer (45), cervical cancer (46) and bladder cancer (47). MTDH is correlated with tumorigenesis and tumour development by regulating cell groWTh, cell cycle, apoptosis, metastasis, epithelial-to-mesenchymal transition, chemoresistance and angiogenesis (48)(49)(50)(51).…”

Section: Discussionmentioning

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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“…MTDH is upregulated in multiple types of human cancer, including breast cancer (29), gastric cancer (30), thyroid carcinoma (31), and cervical cancer (32). MTDH contributes to the regulation of cancer oncogenesis and progression and regulates cell proliferation, cell cycle, apoptosis, metastasis, epithelial-to-mesenchymal transition and angiogenesis (33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑758 inhibits tumorous behavior in tongue squamous cell carcinoma by directly targeting metadherin

Zhang

Zhao

2019

Mol Med Report

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Numerous microRNAs (miRNAs) are dysregulated in tongue squamous cell carcinoma (TSCC), and their dysregulation has been demonstrated to have a strong correlation with TSCC progression via regulation of their targets. Therefore, miRNAs have potential use in the diagnosis and treatment of patients with TSCC. In the present study, miRNA-758 (miR-758) expression in TSCC tissues and cell lines was detected through reverse transcription-quantitative polymerase chain reaction, and the effects of miR-758 on TSCC cell proliferation and invasion were investigated by using Cell Counting kit-8 and Transwell invasion assays. A luciferase reporter assay was performed to determine the target interaction between miR-758 and metadherin (MTDH) in TSCC cells. The results revealed that miR-758 was downregulated in TSCC tissues and cell lines. miR-758 overexpression restricted the proliferation and invasion of TSCC cells. Additionally, MTDH was verified as a direct target gene of miR-758 in TSCC cells. Furthermore, MTDH was observed to be upregulated in TSCC tissues, and the upregulation of MTDH was inversely correlated with miR-758 expression. Moreover, restored MTDH expression significantly counteracted the suppressive effects of miR-758 overexpression on TSCC cells. These results suggested that miR-758 may prevent TSCC progression and development by directly targeting MTDH, thereby providing evidence that miR-758 is a novel therapeutic target for the treatment of patients with TSCC.

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Knockdown of astrocyte elevated gene-1 inhibited cell growth and induced apoptosis and suppressed invasion in ovarian cancer cells

Cited by 16 publications

References 52 publications

<em>let-7d</em> suppresses proliferation and invasion and promotes apoptosis of meningioma by targeting AEG-1

<em>let-7d</em> suppresses proliferation and invasion and promotes apoptosis of meningioma by targeting AEG-1

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

MicroRNA‑758 inhibits tumorous behavior in tongue squamous cell carcinoma by directly targeting metadherin

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