ZNF224, Krüppel like zinc finger protein, induces cell growth and apoptosis-resistance by down-regulation of p21 and p53 via miR-663a

Cho, Jin Gu; Park, Seho; Lim, Chae Hyun; Kim, Hong Sook; Song, Seung Yong; Roh, Tae-Young; Sung, Jong Hwan; Suh, Wonhee; Ham, Seokjin; Lim, Key Hwan; Park, Sang Gyu

doi:10.18632/oncotarget.8870

Cited by 32 publications

(30 citation statements)

References 47 publications

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“…In addition, it is known that ZNF224 primarily localizes to the nucleus and forms a punctate pattern (12). Therefore, we hypothesized that the interaction between ZNF224 and MED28 may occur in the nucleus.…”

Section: Nucleus-specific Interactions Of Znf224 With Med28mentioning

confidence: 96%

“…In a previous study, it was found that ZNF224, a KRAP-ZFP, served a function as a transcriptional repressor upon DNA damage and that the overexpression of ZNF224 results in tumor formation (12). In addition, it was observed that ZNF224 was degraded in a time-dependent manner upon DNA damage (12). Previous studies have revealed that MEDs possess functions as co-repressors or co-activators of transcription in eukaryotic cells (14,22).…”

Section: Nucleus-specific Interactions Of Znf224 With Med28mentioning

confidence: 98%

“…Previously, it was shown that ZNF224 downregulates the transcription of p53 and p21, and that MED28 is localized to the cytosol and nucleus (12,18). In addition, it is known that ZNF224 primarily localizes to the nucleus and forms a punctate pattern (12).…”

Section: Nucleus-specific Interactions Of Znf224 With Med28mentioning

confidence: 99%

“…The primary function of p53 upon DNA damage is to regulate the expression of target genes associated with cell fate (11). A previous study revealed that zinc finger protein 224 (ZNF224) functions as an oncogene in breast cancer cells and downregulates expression of p53 and cyclin dependent kinase 1A (CDK1A, also known as p21) upon DNA damage (12). Although the mRNA expression levels of ZNF224 were unaffected by the DDR, ZNF224 protein levels showed a gradual decrease (12).…”

Section: Introductionmentioning

confidence: 99%

“…A previous study revealed that zinc finger protein 224 (ZNF224) functions as an oncogene in breast cancer cells and downregulates expression of p53 and cyclin dependent kinase 1A (CDK1A, also known as p21) upon DNA damage (12). Although the mRNA expression levels of ZNF224 were unaffected by the DDR, ZNF224 protein levels showed a gradual decrease (12). These results indicated that post-translational modification to ZNF224 or the formation of a complex with another regulatory protein may mediate its inhibition upon DNA damage.…”

Section: Introductionmentioning

confidence: 99%

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MED28 increases the colony‑forming ability of breast cancer cells by stabilizing the ZNF224 protein upon DNA damage

2017

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Abstract. The regulation of gene expression by transcription factors serves a critical function in cell proliferation. Zinc-finger protein 224 (ZNF224), a Krüppel-associated-box-containing zinc finger protein, is known to serve a crucial function in integrating the transcriptional co-factors that activate transcriptional regulation pathways in the cell. A previous study demonstrated that ZNF224 enhances cell proliferation by downregulating the expression of p21 and p53. The present study identified mediator complex subunit 28 (MED28) as a potential binding partner for ZNF224; this was confirmed by co-immunoprecipitation and a surface plasmon resonance assay. Additionally, the KRAB domain at the N-terminal of ZNF224 interacts with the MED domain of MED28. Bimolecular fluorescence complementation analysis revealed that ZNF224 associates with MED28 in the nucleus. In addition, ZNF224 was rapidly degraded upon treatment with the DNA-damaging agent camptothecin (CPT). Transient overexpression of MED28 inhibited the CPT-mediated degradation of ZNF224, resulting in increased colony formation by MCF-7 cells. The molecular mechanisms that underlie the biological outcomes of MED28 expression have not yet been fully elucidated. The present study provides molecular evidence for the function of ZNF224 and MED28 in the DNA-damage response.

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Section: Nucleus-specific Interactions Of Znf224 With Med28mentioning

confidence: 96%

Section: Nucleus-specific Interactions Of Znf224 With Med28mentioning

confidence: 98%

Section: Nucleus-specific Interactions Of Znf224 With Med28mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MED28 increases the colony‑forming ability of breast cancer cells by stabilizing the ZNF224 protein upon DNA damage

2017

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The expression signature of cancer‐associated KRAB‐ZNF factors identified in TCGA pan‐cancer transcriptomic data

et al. 2019

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The KRAB ‐ ZNF (Krüppel‐associated box domain zinc finger) gene family is composed of a large number of highly homologous genes, gene isoforms, and pseudogenes. The proteins encoded by these genes, whose expression is often tissue‐specific, act as epigenetic suppressors contributing to the addition of repressive chromatin marks and DNA methylation. Due to its high complexity, the KRAB ‐ ZNF family has not been studied in sufficient detail, and the involvement of its members in carcinogenesis remains mostly unexplored. In this study, we aimed to provide a comprehensive description of cancer‐associated KRAB ‐ ZNF s using publicly available The Cancer Genome Atlas pan‐cancer datasets. We analyzed 6727 tumor and normal tissue samples from 16 cancer types. Here, we showed that a small but distinctive cluster of 16 KRAB ‐ ZNF s is commonly upregulated across multiple cancer cohorts in comparison to normal samples. We confirmed these observations in the independent panels of lung and breast cancer cell lines and tissues. This upregulation was also observed for most of the KRAB ‐ ZNF splicing variants, whose expression is simultaneously upregulated in tumors compared to normal tissues. Finally, by analyzing the clinicopathological data for breast and lung cancers, we demonstrated that the expression of cancer‐associated KRAB ‐ ZNF s correlates with patient survival, tumor histology, and molecular subtyping. Altogether, our study allowed the identification and characterization of KRAB ‐ ZNF factors that may have an essential function in cancer biology and thus potential to become novel oncologic biomarkers and treatment targets.

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The efficiency of zinc sulfate immersion bath on improved wound healing via promoting antioxidant activity, gene expression biomarkers, and skin re-epithelization in a common carp-induced wound model

El-Adl,

Rezk,

Ali

et al. 2024

Appl Water Sci

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The experiment was designed to examine the influence of employing three doses of ZnSO4 on the wound healing process in partially scaled common carp. A total of 240 healthy common carp fish (52.3 ± 0.9 g) were randomly allocated into four equal groups in triplicate (20 each). The first group left without any zinc sulfate treatment and served as a control group, while the second group through the fourth group were immersed in a zinc sulfate bath at a dose of 2.09, 1.05, and 0.53 mg/L corresponding to 1/5, 1/10, and 1/20 of 96 h LC50 of Zn, (Zn/5, Zn/10, and Zn/20, respectively). After wound induction, tissue specimens were collected within three different intervals (6 h, 24 h, 72 h, and 14 days). The results indicated that the Zn/5 fish group induced doubled folding increments in the expression of transforming growth factor (TGF)‐β1 after 6 h compared to other groups, whereas collagen type I alpha 1 (COL1α1) and metallothionein (Met) genes exhibited a triple folding increment compared to Zn/10 and a fivefold increase compared to control after two days of wound induction. Moreover, vascular endothelial growth factor (VEGF)‐A and fibroblast growth factor (FGF)‐7 genes showed a dose-dependent manner of expression at all examined points after wound induction. Also, all estimated antioxidant biomarker (superoxide-dismutase, SOD; catalase, CAT; glutathione, GSH; and malonaldehyde, MDA) activities were boosted in the Zn/5 group till three days of wound induction compared to all groups. In addition, the reepithelization score and histological alteration results revealed clear improvement in the Zn/5 group, as most muscle fibers appeared regular, straight, and parallel arranged. In contrast, other groups exhibited a detectable limited area of disrupted muscle fibers. Finally, it could be concluded that the ZnSO4 immersion bath at 1/5 of the calculated LC50 effectively enhanced the healing process and skin reepithelization.

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ZNF224, Krüppel like zinc finger protein, induces cell growth and apoptosis-resistance by down-regulation of p21 and p53 via miR-663a

Cited by 32 publications

References 47 publications

MED28 increases the colony‑forming ability of breast cancer cells by stabilizing the ZNF224 protein upon DNA damage

MED28 increases the colony‑forming ability of breast cancer cells by stabilizing the ZNF224 protein upon DNA damage

The expression signature of cancer‐associated KRAB‐ZNF factors identified in TCGA pan‐cancer transcriptomic data

The efficiency of zinc sulfate immersion bath on improved wound healing via promoting antioxidant activity, gene expression biomarkers, and skin re-epithelization in a common carp-induced wound model

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