Progress of cancer research on astrocyte elevated gene-1/Metadherin (Review)

Huang, Yong; Li, Leping

doi:10.3892/ol.2014.2231

Cited by 47 publications

(35 citation statements)

References 97 publications

(175 reference statements)

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“…23,24 As a target of Ras, MTDH activates multiple oncogenic signaling pathways including phosphoinositide-3 kinase (PI3K)-Akt, mitogen-activated protein kinase (MAPK), Wnt, and NF-kB involved in regulation of proliferation, invasion, chemoresistance, angiogenesis, and metastasis. [25][26][27][28] In particular, MTDH showed higher expression, compared with that in normal brain tissues, in tumors of the CNS, such as neuroblastoma, glioblastoma multiforme, and oligodendroglioma.…”

Section: Discussionmentioning

confidence: 99%

MiR-302c-3p suppresses invasion and proliferation of glioma cells via down-regulating metadherin (MTDH) expression

Wang

Wei

Tong

et al. 2015

Cancer Biology & Therapy

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Glioma is the most common malignant brain tumors with poor prognosis. The molecular events involved in the development and progression of glioma remain unclear. In this study, the expression levels of miR-302c-3p were examined in glioma tissues by qRT-PCR. The in vitro and in vivo functional effects of miR-302c-3p were examined further. Luciferase reporter assays were conducted to confirm the targeting associations. Results showed that the expression level of miR-302c-3p in glioma tissues was significantly lower than those in normal brain tissues (P < 0.001). The decreased expression of mi-302c-3p in glioma was positively associated with WHO grade (P < 0.001). Up-regulation of MTDH was also detected in glioma tumors compared with normal brain tissues (P = 0.0027) and is inversely correlated with miR-302c-3p expression (P = 0.003, R(2) = 0.4065). MTDH mRNA is a direct target of miR-302c-3p, whose ectopic expression decreases MTDH expression through binding to its 3'-untranslated region. Overexpression of miR-302c-3p results in a dramatic inhibition of glioma cells proliferation and invasion in vitro and in vivo. These data suggest that miR-302c-3p play a pivotal role in the progression of glioma by targeting MTDH and is a potential inhibitor in glioma treatment.

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Section: Discussionmentioning

confidence: 99%

MiR-302c-3p suppresses invasion and proliferation of glioma cells via down-regulating metadherin (MTDH) expression

Wang

Wei

Tong

et al. 2015

Cancer Biology & Therapy

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“…[16][17][18][19][20] The expression level of AEG-1 is aberrantly high in melanoma. 21,22 Clinical studies showed that elevated expression of AEG-1 was associated with tumour progression and poor prognosis of melanoma. 22However, the exact role of AEG-1 in melanoma cells is not clear.…”

mentioning

confidence: 99%

Silencing of astrocyte elevated gene‐1 inhibits proliferation and migration of melanoma cells and induces apoptosis

Zhang

Peng

Wang

et al. 2017

Clin Exp Pharma Physio

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Melanoma is an aggressive skin malignancy with a high mortality. Astrocyte elevated gene-1 (AEG-1), a downstream target of Ras and c-Myc, has been implicated in the development of multiple tumours, but its role in melanoma remains unclear. In the present study, the role of AEG-1 in melanoma was explored through AEG-1 silencing. Our results showed that silencing AEG-1 inhibited the proliferation of melanoma cells, induced cell cycle arrest, and reduced levels of cyclin A, cyclin B, cyclin D1, cyclin E, and cyclin-dependent kinase 2. AEG-1silencing also induced apoptosis in melanoma cells and altered the levels of cleaved caspase-3, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein. Moreover, silencing AEG-1 suppressed the migration and invasion of melanoma cells, reduced the expressions and activities of matrix metallopeptidase (MMP)-2 and MMP-9, and inhibited the activation of the Wnt/β-catenin signalling pathway in melanoma cells. Furthermore, in vivo experiments revealed that AEG-1 silencing inhibited the growth of melanoma xenografts in nude mice. In summary, our study demonstrates an oncogenic role of AEG-1 in melanoma and suggests that AEG-1 may serve as a potential therapeutic target in the treatment of melanoma.

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“…PI3K/Akt signaling primarily exerts anti-apoptotic effects by affecting multiple downstream effector molecules (34). Knockout of PI3K, Akt and associated genes by genetic intervention, or inhibition by small molecule drugs, which blocks the activation of downstream anti-apoptotic effector molecules and promotes apoptosis, has become a key focus of research on cancer treatment (35). The results of the present study suggested that psoralidin was able to reduce the protein expression levels of PI3K and Akt in Eca9706 cells; however, upregulation of PI3K protein expression reduced the viability of Eca9706 cells.…”

Section: Discussionmentioning

confidence: 99%

Psoralidin inhibits proliferation and enhances apoptosis of human esophageal carcinoma cells via NF-κB and PI3K/Akt signaling pathways

et al. 2016

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Abstract. Esophageal cancer is the most common gastrointestinal cancer. Psoralidin exhibits antioxidant, anti-apoptotic, anti-inflammatory and antitumor effects, which result in the inhibition of cancer formation. The present study aimed to investigate the effect of psoralidin on esophageal carcinoma proliferation and growth, and to elucidate its underlying mechanism of action. The effect of psoralidin on cell proliferation was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium brom ide assay. Using a n a n nexin V-f luorescein isothiocyanate/propidium iodide apoptosis detection kit and 4' ,6-diamidino-2-phenylindole staining assay, the present study demonstrated that psoralidin significantly enhanced apoptosis of human esophageal carcinoma Eca9706 cells. In addition, caspase-3 activity was analyzed with a caspase-3 colorimetric assay kit, while nuclear factor (NF)-κB activity and protein phosphatidylinositol 3-kinase (PI3K)/Akt expression were measured with an NF-κB enzyme-linked immunosorbent assay kit and western blot analysis, respectively. Eca9706 cells were treated with a PI3K agonist in order to investigate the mechanism of action of psoralidin. It was observed that psoralidin was able to decrease the proliferation and promote the cellular apoptosis of Eca9706 cells in a dose-dependent manner. Furthermore, psoralidin was also able to inhibit the caspase-3 activity of Eca9706 cells in a dose-dependent manner. In addition, psoralidin inhibited NF-κB activity and reduced PI3K and Akt protein expression in Eca9706 cells. Notably, the PI3K agonist was able to reverse the effect of psoralidin on Eca9706 cells. The results of the present study demonstrated that psoralidin was able to inhibit proliferation and enhance apoptosis of human esophageal carcinoma cells via the NF-κB and PI3K/Akt signaling pathways.

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Progress of cancer research on astrocyte elevated gene-1/Metadherin (Review)

Cited by 47 publications

References 97 publications

MiR-302c-3p suppresses invasion and proliferation of glioma cells via down-regulating metadherin (MTDH) expression

MiR-302c-3p suppresses invasion and proliferation of glioma cells via down-regulating metadherin (MTDH) expression

Silencing of astrocyte elevated gene‐1 inhibits proliferation and migration of melanoma cells and induces apoptosis

Psoralidin inhibits proliferation and enhances apoptosis of human esophageal carcinoma cells via NF-κB and PI3K/Akt signaling pathways

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