[Mechanism of ING4 mediated inhibition of the proliferation and migration of human glioma cell line U251].
ABSTRACT To investigate the effect of Ad-ING4 on proliferation and migration of glioma cells and explore its probable mechanism.
U251 were infected with Ad-ING4. ING4 gene expression was evaluated by RT-PCR. MTT assay was adopted to evaluate the effect of ING4 on proliferation of U251; Boyden chamber assay was used to check the effect of ING4 on the migration of U251. In ING4 transfected U251, Western blot was used for detecting NGF and TrkA expression; Pull-down assay was used for detecting active RhoA expression.
ING4 was overexpressed in Ad-ING4 transfected U251 cells. ING4 inhibited proliferation and migration of U251 significantly. Moreover, overexpression of ING4 result in depression of NGF, TrkA and active RhoA.
ING4 mediated inhibition of the proliferation and migration of human glioma cells by down regulating NGF, TrkA and active RhoA expression.
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ABSTRACT: The ING4 tumor suppressor plays a significant role in various cancer-related cellular processes. AUF1 affects the stability and/or translation of multiple mRNAs via binding to an AU-rich element in the 3'-untranslated regions. In this study, we identify AUF1 as a novel and direct binding partner of ING4. mRNP immunoprecipitation assays indicated that ING4, AUF1 and MYC mRNA present in the same mRNP complex. ING4 suppressed MYC protein expression without altering MYC mRNA levels, and abolished the cell proliferation induced by AUF1 in K562 cells. These results suggest that ING4 may regulate MYC translation by its association with AUF1. STRUCTURED SUMMARY OF PROTEIN INTERACTIONS: ING4bindstoAUF1 p40bypull down(View interaction) ING4physically interactswithAUF1byanti tag coimmunoprecipitation(View Interaction:1,2) ING4bindstoAUF1 p37bypull down(View Interaction:1,2) ING4bindstoAUF1 p42bypull down(View interaction) ING4bindstoAUF1 p45bypull down(View interaction) ING4physically interactswithAUF1 byanti bait coimmunoprecipitation(View Interaction:1,2,3,4,5,6) ING4bindstoAUF1bypull down(View interaction).FEBS letters 04/2013; 587(11). DOI:10.1016/j.febslet.2013.04.004 · 3.34 Impact Factor
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ABSTRACT: There is growing evidence that inhibitor of growth 4 (ING4) plays a pivotal role in development and progression of multiple different tumors; however, its precise function in gastric carcinoma remains to be elucidated. In the present study, we investigated ING4 level in gastric carcinoma tissues and cells, and preliminarily elucidated the role of ING4 in the proliferation and invasion of gastric carcinoma. The results demonstrated that expressions of ING4 mRNA and protein in gastric carcinoma tissues and cells were significantly lower than those in normal tissues and cells (P < 0.05). ING4 level in gastric carcinoma cells stably expressing ING4 was markedly higher than those in untreated group and empty vector pcDNA3.1 group (P < 0.05). Elevated ING4 level resulted in the inhibition of proliferation and invasion in three of gastric carcinoma cell lines MKN-28, SGC-7901 and MKN-45. Most notably, increased ING4 level evidently evoked the down-regulation of p65, p-IκBα, MMP-9 and uPA proteins and the up-regulation of IκBα protein. Our results presented herein suggest that ING4 level elevation mediated proliferation and invasion inhibition may be tightly associated with the suppression of NF-κB signaling pathway.Molecular Biology Reports 09/2013; 40(10). DOI:10.1007/s11033-013-2675-3 · 1.96 Impact Factor
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ABSTRACT: Inhibitor of growth 4 (ING4) is a tumor suppressor that can inhibit cell growth and induce apoptosis. ING4 expression levels show negative correlation with the clinical stage, histological grade, and lymph node metastasis of colorectal cancer. Further insights are needed to analyze the effect of adenovirus-mediated ING4 on colorectal cancer cell growth and the response to paclitaxel treatment. In this study, we found adenovirus-mediated ING4 expression reduced proliferation and enhanced apoptosis in the SW1116 cells. p-Stat3 and Ki-67 expression significantly decreased in the SW1116 cells treated with Ad-ING4, PTX, or Ad-ING4 + PTX compared with those treated with PBS or Ad-GFP both in vitro and in vivo (P < 0.05). In animal experiments, the mice treated with Ad-ING4, PTX, or Ad-ING4 + PTX exhibited significantly inhibited growth of SW1116 xenografts compared with those treated with PBS or Ad-GFP (P < 0.05) and the combination (Ad-ING4 + PTX) treatment exhibited the highest inhibition. Our results highlight that Ad-ING4 significantly inhibits growth and induces apoptosis in SW1116 colorectal cancer cells and suppresses tumor growth in SW1116 xenografts by downregulating p-Stat3 and Ki-67 expression. A combination of Ad-ING4 and PTX exhibits the highest inhibition, indicating that ING4 enhances sensitivity to chemotherapy.International journal of clinical and experimental pathology 01/2015; 8(3):2919-27. · 1.78 Impact Factor