ING function in apoptosis in diverse model systemsThis paper is one of a selection of papers published in this Special Issue, entitled CSBMCB’s 51st Annual Meeting – Epigenetics and Chromatin Dynamics, and has undergone the Journal’s usual peer review process.

Shah, Sitar; Smith, Heather; Feng, Xiaolan; Rancourt, Derrick E.; Riabowol, Karl

doi:10.1139/o08-107

Cited by 30 publications

(22 citation statements)

References 34 publications

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“…In addition, it was reported that ING5 could affect adhesion, migration, invasion, proliferation and apoptosis of tumor cells [18, 25–34]. Bax and GADD45 were ING5 target apoptotic genes [35, 36]. The anti-proliferative effect of ING5 depended on its interaction with INCA1 [37].…”

Section: Discussionmentioning

confidence: 99%

“…It was worth noting that ING5-mediated chemoresistance was closely related to their apoptotic resistance, Akt activation, and the over-expression of chemoresistance-related genes [18, 26, 30]. For the inhibiting effect on epithelial-mesenchymal transition (EMT), ING5 inhibited lung cancer aggressiveness [27], and ING5 suppressed PI3K/Akt in breast cancer [36]. In spite of these the correlation between ING5 and ovarian cancer still remained unclear.…”

Section: Discussionmentioning

confidence: 99%

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MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression

et al. 2017

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BackgroundWe aimed to investigate the function of miR-1307 in chemoresistance and to explore its chemoresistance mechanism in ovarian cancer.MethodsIC50 determination was used to test the chemoresistance profling in ovarian cancer cells. QRT-PCR or western blot was used to validate the expression level of miR-1307 and candidate gene or protein. Colony formation assay and FITC-labeled enhanced Annexin V immunofluorescence were used to compare cell proliferation and apoptosis ability, respectively. The potential target gene and its biological function of miRNA-1307 were also analyzed. Bioinformatics and Luciferase Reporter Gene Assay were conducted to validate the regulation of miRNA-1307 on the ING5 expression. Xenografts assay was used to demonstrate the inhibiting effect of miR-1307 ASO and Taxol therapy against ovarian cancer in vivo.ResultsMiR-1307 was over-expressed in chemoresistant ovarian cancer cell line A2780/Taxol, and over-expression or loss of miR-1307 promoted or inhabited chemoresistance. And we also found that the over-expression of miR-1307 promoted proliferation and inhibited apoptosis in ovarian cancer cells. Besides, we demonstrated that ING5 was a direct target of miR-1307 and miR-1307 down-regulated the ING5 expression in ovarian cancer cells. Additionally, we showed that ING5 inhibited cell proliferation, promoted cell apoptosis and inhabited chemoresistance reversely. Furthermore, the up-regulated ability of cell apoptosis and down-regulated ability of chemoresistance following the loss of miR-1307 was reversed by adding ING5 siRNA in vitro. Finally, we proved the inhibiting effect of miR-1307 ASO and Taxol therapy by increasing the ING5 expression against ovarian cancer through xenografts assay in vivo.ConclusionOur results suggested that miR-1307 could promote ovarian cancer chemoresistance by targeting the ING5 expression and miR-1307 might serve as a therapeutic target for ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression

et al. 2017

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“…The latter promotes DNA replication via the interaction with mini-chromosome maintenance protein because ING5 knockdown completely abolishes DNA synthesis, and HBO1 knockdown increases S-phase cells ratio [8]. ING5 was reported to activate the cyclin-dependent kinase inhibitor p21/waf1 promoter and acetylated ING5 subsequently bound to the promoters of its target apoptotic genes, including Bax and GADD45 [9, 10]. The antiproliferative effect of ING5 depended on its interaction with INCA1 [11].…”

Section: Introductionmentioning

confidence: 99%

The down-regulated ING5 expression in lung cancer: A potential target of gene therapy

et al. 2016

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ING5 can interact with p53, thereby inhibiting cell growth and inducing apoptosis. We found that ING5 overexpression not only inhibited proliferation, migration, and invasion, but also induced G2 arrest, differentiation, autophagy, apoptosis, glycolysis and mitochondrial respiration in lung cancer cells. ING5 transfection up-regulated the expression of Cdc2, ATG13, ATG14, Beclin-1, LC-3B, AIF, cytochrome c, Akt1/2/3, ADFP, PFK-1 and PDPc, while down-regulated the expression of Bcl-2, XIAP, survivin,β-catenin and HXK1. ING5 transfection desensitized cells to the chemotherapy of MG132, paclitaxel, and SAHA, which paralleled with apoptotic alteration. ING5 overexpression suppressed the xenograft tumor growth by inhibiting proliferation and inducing apoptosis. ING5 expression level was significantly higher in normal tissue than that in lung cancer at both protein and mRNA levels. Nuclear ING5 expression was positively correlated with ki-67 expression and cytoplasmic ING5 expression. Cytoplasmic ING5 expression was positively associated with lymph node metastasis, and negatively with age, lymphatic invasion or CPP32 expression. ING5 expression was different in histological classification: squamous cell carcinoma > adenocarcinoma > large cell carcinoma > small cell carcinoma. Taken together, our data suggested that ING5 downregulation might involved in carcinogenesis, growth, and invasion of lung cancer and could be considered as a promising marker to gauge the aggressiveness of lung cancer. It might be employed as a potential target for gene therapy of lung cancer.

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“…Down regulation of most of the INGs has been reported in many different tumor types [4][5][6][7][8]. ING proteins are highly conserved in vertebrates and are also found in distantly related organisms such as worms and yeast [9]. Based upon bioinformatic analyses of all sequences found showing homology to human ING proteins, a number of domains and motifs have been identified and subsequently characterized [10].…”

Section: Domains Of the Inhibitors Of Growth (Ing)mentioning

confidence: 99%

“…ING3 has the highest sequence similarity to its human homologue, ING3, compared to the other ING proteins [9]. In a recent study, the function of ing-3 was examined in regards to its relationship with cep-1, the C. elegans p53 homologue, in pathways relevant to apoptosis.…”

Section: Ing3 Ablation In Caenorhabditis Elegansmentioning

confidence: 99%

Signaling Pathways of the ING Proteins in Apoptosis

Shah

Riabowol²

2009

CDT

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Members of the ING family of type II tumor suppressors reside in different chromatin regulatory complexes and are stoichiometeric members of histone acetyltransferase (HAT) and histone deacetylase (HDAC) complexes. It has been frequently observed that expressing ING proteins promotes apoptosis in both normal and transformed cells of different species. They have also been reported to either rely upon p53, or to add to its ability to promote programmed cell death (apoptosis) although whether ING proteins require p53 to induce apoptosis is now questionable based upon observations using knockout cell lines and animal models. Genetic studies in model organisms, and particularly in Caenorhabditis elegans, have identified different pathways involved in apoptosis during development, in the germ line and in response to various forms of stress including DNA damage. In this review we summarize structural features of the INGs and recent observations made in knockout models of Mus musculus and Caenorhabditis elegans that have helped to further clarify the functions of the ING proteins in biochemical pathways leading to apoptosis. Based upon these observations we propose a model for how ING proteins may act both independently and in concert with p53 to promote apoptosis.

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ING function in apoptosis in diverse model systemsThis paper is one of a selection of papers published in this Special Issue, entitled CSBMCB’s 51st Annual Meeting – Epigenetics and Chromatin Dynamics, and has undergone the Journal’s usual peer review process.

Cited by 30 publications

References 34 publications

MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression

MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression

The down-regulated ING5 expression in lung cancer: A potential target of gene therapy

Signaling Pathways of the ING Proteins in Apoptosis

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