Overexpression of the human <i>ZNF300</i> gene enhances growth and metastasis of cancer cells through activating NF‐<i>k</i>B pathway

Wang, Tao; Wang, Xianguo; Xu, Junhua; Wu, Xiang-Peng; Qiu, Hongling; Yi, Hong; Li, Wenxin

doi:10.1111/j.1582-4934.2011.01388.x

Cited by 41 publications

(34 citation statements)

References 39 publications

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“…Nonetheless, using both knockdown and overexpression strategies, we found that ZNF367 inhibited cancer growth and invasion, which suggests that the elevated levels in cancer samples are counter-regulatory and inhibit cancer progression. This finding is consistent with recent studies showing the diverse functions of other ZNF proteins in cancer biology and in mediating resistance to chemotherapy [9], [10], [13]-[15]. Moreover, we demonstrate that the increased levels of ZNF367 are likely a result of a loss in expression of miR-195.…”

Section: Discussionsupporting

confidence: 93%

ZNF367 Inhibits Cancer Progression and Is Targeted by miR-195

et al. 2014

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BackgroundSeveral members of the zinc finger protein family have been recently shown to have a role in cancer initiation and progression. Zinc finger protein 367 (ZNF367) is a member of the zinc finger protein family and is expressed in embryonic or fetal erythroid tissue but is absent in normal adult tissue.Methodology/Principal FindingsWe show that ZNF367 is overexpressed in adrenocortical carcinoma, malignant pheochromocytoma/paraganglioma and thyroid cancer as compared to normal tissue and benign tumors. Using both functional knockdown and ectopic overexpression in multiple cell lines, we show that ZNF367 inhibits cellular proliferation, invasion, migration, and adhesion to extracellular proteins in vitro and in vivo. Integrated gene and microRNA expression analyses showed an inverse correlation between ZNF367 and miR-195 expression. Luciferase assays demonstrated that miR-195 directly regulates ZNF367 expression and that miR-195 regulates cellular invasion. Moreover, integrin alpha 3 (ITGA3) expression was regulated by ZNF367.Conclusions/SignificanceOur findings taken together suggest that ZNF367 regulates cancer progression.

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Section: Discussionsupporting

confidence: 93%

ZNF367 Inhibits Cancer Progression and Is Targeted by miR-195

et al. 2014

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“…Other studies suggest that the NF‐κB pathway is involved in regulation of directional migration . The NF‐κB pathway widely participates in gene expression and regulation of chemokines, cytokines and adhesion molecules . The IκB kinase (IKK) complex consists of two catalytic subunits (IKK‐α and IKK‐β) and a regulatory subunit (IKK‐γ/NEMO).…”

Section: Discussionmentioning

confidence: 99%

TNF‐α promotes survival and migration of MSCs under oxidative stress via NF‐κB pathway to attenuate intimal hyperplasia in vein grafts

Bai

et al. 2017

J Cellular Molecular Medi

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The oxidative stress caused by endothelial injury is involved in intimal hyperplasia (IH) in vein grafts. Mesenchymal stem cells (MSCs) can home to injured intima and promote endothelial repair. However, MSC apoptosis is increased accompanied by decreased functional activity under oxidative stress. Thus, we investigate whether tumour necrosis factor‐α (TNF‐α) can promote the survival and activity of MSCs under oxidative stress to reduce IH more effectively, and establish what role the NF‐κB pathway plays in this. In this study, we preconditioned MSCs with TNF‐α (TNF ‐α‐PCMSCs) for 24 hrs and measured the activation of the IKK/NF‐κB pathway. EdU and transwell assays were performed to assess proliferation and migration of TNF ‐α‐PCMSCs. Apoptosis and migration of TNF ‐α‐ PCMSCs were evaluated in conditions of oxidative stress by analysis of the expression of Bcl‐2 and CXCR4 proteins. TNF ‐α‐ PCMSCs were transplanted into a vein graft model, so that cell homing could be tracked, and endothelial apoptosis and IH of vein grafts were measured. The results demonstrated that TNF‐α promotes proliferation and migration of MSCs. Furthermore, survival and migration of TNF ‐α‐ PCMSCs under oxidative stress were both enhanced. A greater number of MSCs migrated to the intima of vein grafts after preconditioning with TNF‐α, and the formation of neointima was significantly reduced. These effects could be partially abolished by IKK XII (NF‐κB inhibitor). All these results indicate that preconditioning with TNF‐α can promote survival and migration of MSCs under oxidative stress via the NF‐κB pathway and thus attenuate IH of vein grafts.

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“…The ZNF300 SNP rs4958427 was associated with immediate reactions to BL in the Spanish population but not in the Italian population. This gene encodes a transcription factor involved in the NF-κB signaling pathway and could have an effect on HLA-DRA expression [25]. In addition, this gene, together with NOD1 and NOD2, has been strongly associated with inflammation in Crohn disease [26].…”

Section: Immediate Reactions To Bl Antibioticsmentioning

confidence: 99%

Update on the Genetic Basis of Drug Hypersensitivity Reactions

Jurado‐Escobar¹,

Perkins²,

García‐Martín³

et al. 2017

J Investig Allergol Clin Immunol

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Drug hypersensitivity reactions (DHRs) are unpredictable, complex responses to medicines in predisposed individuals. They represent a major health problem owing to the number of patients affected and the severity of the clinical conditions they can induce. In addition to environmental factors, the underlying mechanisms of DHRs are also influenced by genetic factors, although considerable gaps remain in our knowledge. Therefore, further study of the genetics of DHRs is necessary to shed light on their underlying mechanisms. In this manuscript, we provide an update on the genetic basis of the most frequent types of DHRs, including those mediated by immunological and nonimmunological mechanisms. For the first group, we will focus on immediate reactions to β-lactam antibiotics, which are associated mainly with the IgE pathway (IL13, IL4R, LGALS3, and NOD2) and antigen presentation (HLA-DRA), and nonimmediate reactions to allopurinol, anticonvulsants, antibiotics, and antiretrovirals, which are often associated with polymorphisms in the HLA system. For the second group, we will focus on nonsteroidal anti-inflammatory drugs, which are mostly associated with genetic variants in enzymes and receptors from the arachidonic acid pathway (eg, ALOX5, ALOX5AP, PTGDR, and CYSLTR1). The information provided here will be of interest for medical practitioners from a range of disciplines who come across these reactions in their clinical practice, as well as for allergologists. Key words: Drug hypersensitivity. Immunologically-mediated reactions. Cross-hypersensitivity. Single-nucleotide polymorphisms. Genomewide association study. ResumenLas reacciones de hipersensibilidad a fármacos (RHFs) son respuestas no predecibles que se producen en algunos sujetos y que representan un serio problema de salud pública debido al número de pacientes implicados y a su potencial gravedad. Además de factores ambientales, en estas reacciones también participan factores genéticos, cuya influencia está, en la mayoría de los casos, aún por dilucidar. En este manuscrito describiremos la información disponible sobre la base genética de los tipos más frecuentes de RHFs, tanto de las mediadas inmunológicamente como de aquellas en las que no se requiere reconocimiento antigénico. En el primer grupo nos ocuparemos de las reacciones inmediatas a antibióticos β-lactámicos, que han sido asociadas con variantes relacionadas con la IgE (IL13, IL4R, LGALS3 y NOD2) y la presentación antigénica (HLA-DRA), y de las reacciones no inmediatas a diferentes grupos de medicamentos (alopurinol, anticonvulsivos, antibióticos y antiretrovirales), relacionadas fundamentalmente con polimorfismos en el sistema HLA. En el segundo grupo nos centraremos en las reacciones inducidas por antiinflamatorios no esteroideos (AINE), que han sido asociadas básicamente con variantes en enzimas y receptores de la vía del ácido araquidónico (ALOX5, ALOX5AP, PTGDR y CYSLTR1, entre otros). Esta revisión puede ser de interés no sólo para alergólogos, sino para los profesionales de otras ...

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Overexpression of the human ZNF300 gene enhances growth and metastasis of cancer cells through activating NF‐kB pathway

Cited by 41 publications

References 39 publications

ZNF367 Inhibits Cancer Progression and Is Targeted by miR-195

ZNF367 Inhibits Cancer Progression and Is Targeted by miR-195

TNF‐α promotes survival and migration of MSCs under oxidative stress via NF‐κB pathway to attenuate intimal hyperplasia in vein grafts

Update on the Genetic Basis of Drug Hypersensitivity Reactions

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