Tip60 regulates MT1-MMP transcription and invasion of glioblastoma cells through NF-κB pathway

Takino, Takahisa; Nakada, Mitsutoshi; Li, Zi‐Chen; Yoshimoto, T.; Domoto, Takahiro; Sato, Hiroshi

doi:10.1007/s10585-015-9756-8

Cited by 20 publications

(14 citation statements)

References 33 publications

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“…In addition, NFKBIA is an NFκB inhibitor which inhibits the activity of dimeric NF-kappa-B/REL complexes 62 , suggesting a possible mechanism by which H4K12ac modulates MCP2/CCL8 expression. To further analyzed the signaling mechanisms depicted in the in silico analysis, it may be worth directly targeting H4K12ac with siRNA or CRISPR Cas9 techniques to block TIP60 histone acetyl transferase as previously described 63 , 64 .…”

Section: Discussionmentioning

confidence: 99%

Novel detection of post-translational modifications in human monocyte-derived dendritic cells after chronic alcohol exposure: Role of inflammation regulator H4K12ac

Parira

Figueroa

Laverde

et al. 2017

Sci Rep

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Previous reports on epigenetic mechanisms involved in alcohol abuse have focus on hepatic and neuronal regions, leaving the immune system and specifically monocyte-derived dendritic cells (MDDCs) understudied. Our lab has previously shown histone deacetylases are modulated in cells derived from alcohol users and after in vitro acute alcohol treatment of human MDDCs. In the current study, we developed a novel screening tool using matrix assisted laser desorption ionization-fourier transform-ion cyclotron resonance mass spectrometry (MALDI-FT-ICR MS) and single cell imaging flow cytometry to detect post-translational modifications (PTMs) in human MDDCs due to chronic alcohol exposure. Our results demonstrate, for the first time, in vitro chronic alcohol exposure of MDDCs modulates H3 and H4 and induces a significant increase in acetylation at H4K12 (H4K12ac). Moreover, the Tip60/HAT inhibitor, NU9056, was able to block EtOH-induced H4K12ac, enhancing the effect of EtOH on IL-15, RANTES, TGF-β1, and TNF-α cytokines while restoring MCP-2 levels, suggesting that H4K12ac may be playing a major role during inflammation and may serve as an inflammation regulator or a cellular stress response mechanism under chronic alcohol conditions.

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Section: Discussionmentioning

confidence: 99%

Novel detection of post-translational modifications in human monocyte-derived dendritic cells after chronic alcohol exposure: Role of inflammation regulator H4K12ac

Parira

Figueroa

Laverde

et al. 2017

Sci Rep

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“…The importance of MMPs and TIMPs for tumor progression has been demonstrated in different types of primary and metastatic brain tumors. The expression of a variety of MMPs, including MMP‐2 (Komatsu et al, ), MMP‐3 (Bodey et al, ), MMP‐9 (Nordqvist et al, ; Komatsu et al, ), MMP‐10 (Bodey et al, ), MMP‐13 (Guan et al, ), and MMP‐14 (Takino et al, ), was shown to be associated with a more aggressive behavior in primary brain tumors such as glioblastoma, astrocytoma, and meningioma. Similarly, different MMPs including MMP‐1 (Wu et al, ) and MMP‐2 (Rojiani et al, ) as well as TIMPs such as TIMP‐1(Rojiani et al, ) were overexpressed in brain metastases from lung and breast cancer.…”

Section: Diagnosis and Prognosis Of Cancers By Mmpsmentioning

confidence: 99%

Metalloproteinases and their roles in human cancer

Roy

Morad

Jedinak

et al. 2019

The Anatomical Record

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It is now widely appreciated that members of the matrix metalloproteinase (MMP) family of enzymes play a key role in cancer development and progression along with many of the hallmarks associated with them. The activity of these enzymes has been directly implicated in extracellular matrix remodeling, the processing of growth factors and receptors, the modulation of cell migration, proliferation, and invasion, the epithelial to mesenchymal transition, the regulation of immune responses, and the control of angiogenesis. Certain MMP family members have been validated as biomarkers of a variety of human cancers including those of the breast, brain, pancreas, prostate, ovary, and others. The related metalloproteinases, the A disintegrin and metalloproteinases (ADAMs), share a number of these functions as well. Here, we explore these essential metalloproteinases and some of their disease-associated activities in detail as well as some of their complementary translational potential. Anat Rec, 303:1557-1572, 2020.Matrix metalloproteinases (MMPs) are a multigene family of metal-dependent endopeptidases that play important and diverse roles in normal physiological and pathological processes. The classic domain structure of MMP family members can be found in Figure 1 (Roy et al., 2009). MMPs include an amino-terminal signal peptide required for secretion, a pro-domain that mediates latency via a cysteine-switch mechanism and a Zn 2+ -dependent catalytic domain that is responsible for enzymatic function. A majority of MMPs also contain a C-terminal hemopexinlike domain that provides substrate specificity. MMP activity is the rate-limiting step in extracellular matrix (ECM) degradation and it can regulate the activity of other proteases, growth factors, cytokines, and cell-surface ligands

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“…Tip60 has been shown to remodel chromatin in several diseases, including several cancers such as lymphoma, melanoma, breast, colon, and lung cancer [28]. Many studies have shown that Tip60 may function as a tumor suppressor [29,30]. Hu et al reported that during the blastocyst stage of development, lack of Tip60 promoted embryo lethality, showing that Tip60 is an essential gene [31].…”

Section: Tip60 Attenuated the Proliferation And Metastasis Of Cca Celmentioning

confidence: 99%

Tip60 Suppresses Cholangiocarcinoma Proliferation and Metastasis via PI3k-AKT

Zhang¹,

Han²,

Shao³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Aberrant expression of Tip60 is associated with progression in many cancers. However, the role of Tip60 in cancer progression remains contradictory. The aim of this study was to investigate the clinical significance, biological functions and underlying mechanisms of Tip60 deregulation in cholangiocarcinoma (CCA) for the first time. Methods: Quantitative real-time PCR (QRT-PCR), western blotting and immunohistochemistry staining (IHC) were carried out to measure Tip60 expression in CCA tissues and cell lines. Kaplan–Meier analysis and the log-rank test were used for survival analysis. In vitro, cell proliferation was evaluated by flow cytometry and CCK-8, colony formation, and EDU assays. Migration/ invasion was evaluated by trans-well assays. Phosphokinase array was used to confirm the dominant signal regulated by Tip60. Tumor growth and metastasis were demonstrated in vivo using a mouse model. Results: Tip60 was notably downregulated in CCA tissues, which was associated with greater tumor size, venous invasion, and TNM stage. Down-regulation of Tip60 was associated with tumor progression and poorer survival in CCA patients. In vitro and in vivo studies demonstrated that Tip60 suppressed growth and metastasis throughout the progression of CCA. We further identified the PI3K/AKT pathway as a dominant signal of Tip60 and suggested that Tip60 regulated CCA cell proliferation and metastasis via PT3K-AKT pathway. Pearson analysis revealed that PTEN was positively correlated with the Tip60 level in CCA tissues. Conclusion: Tip60, as a tumor suppressor in CCA via the PI3K/AKT pathway, might be a promising therapeutic target or prognostic marker for CCA.

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Tip60 regulates MT1-MMP transcription and invasion of glioblastoma cells through NF-κB pathway

Cited by 20 publications

References 33 publications

Novel detection of post-translational modifications in human monocyte-derived dendritic cells after chronic alcohol exposure: Role of inflammation regulator H4K12ac

Novel detection of post-translational modifications in human monocyte-derived dendritic cells after chronic alcohol exposure: Role of inflammation regulator H4K12ac

Metalloproteinases and their roles in human cancer

Tip60 Suppresses Cholangiocarcinoma Proliferation and Metastasis via PI3k-AKT

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