Ask about this productRelated genes to: ZNF570 antibody
- Gene:
- ZNF570 NIH gene
- Name:
- zinc finger protein 570
- Previous symbol:
- -
- Synonyms:
- FLJ30791
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-15
- Date modifiied:
- 2014-11-18
Related products to: ZNF570 antibody
Related articles to: ZNF570 antibody
- The hormone receptors (HR) + /human epidermal growth factor receptor 2 (HER2) - subtype accounts for 60%-70% of primary breast cancer (BC) cases. Tamoxifen (TAM) has been the first-line endocrine therapeutic agent for this subtype for over 30 years and induces clinical responses in more than 70% of estrogen receptor-positive (ER +) tumors. However, 22%-52% of patients develop tumor recurrence or distant metastasis due to acquired tamoxifen resistance, which highlights the critical need to explore resistance mechanisms as well as identify new therapeutic targets for improving patient prognosis. The objective is to examine the role of ZNF570 in tamoxifen resistance of ER + BC. Analyses of The Cancer Genome Atlas (TCGA) database coupled with validation with clinical samples indicated that ZNF570 is overexpressed in HR + BC. Importantly, ZNF570 expression is linked to a poorer patient prognosis and serves as an independent prognostic indicator for HR + BC. Furthermore, ZNF570 expression is significantly higher in tumor tissues from tamoxifen-resistant patients than in those from tamoxifen-sensitive patients. Tamoxifen-resistant cell models (MCF7-TAM and T47D-TAM) were established by continuously exposing MCF-7 and T47D cells to tamoxifen for induction. These models demonstrated that ZNF570 expression is higher in resistant cells than their parental counterparts, and this expression level exhibits a positive link with estrogen receptor alpha (ERα) expression levels. Functional experiments demonstrated that ZNF570 knockout in tamoxifen-resistant cells significantly increased the cells' sensitivity to tamoxifen and reduced ER expression. Conversely, ZNF570 overexpression in parental MCF-7 as well as T47D cells decreased cells' sensitivity to tamoxifen and increased ER expression. Furthermore, ZNF570 was found to promote proliferation, invasion, and migration of ER + BC cells. Tumor-promoting effect of ZNF570 in vivo was validated by nude mouse xenograft experiments. Mechanistically, proteomic analyses and combined in vitro as well as in vivo experiments verified that ZNF570 knockout reverses tamoxifen resistance by activating ferroptosis. This ferroptosis activation is mediated by downregulating the expression of glutathione peroxidase 4 (GPX4) coupled with cystine/glutamate transporter (XCT), upregulating the expression of tumor protein p53 (TP53), rising intracellular levels of reactive oxygen species (ROS), ferrous ions (Fe⁺), and malondialdehyde (MDA), and decreasing intracellular content of reduced glutathione (GSH). In contrast, ZNF570 overexpression inhibits ferroptosis. In conclusion, ZNF570 promotes tamoxifen resistance in ER + BC cells by enhancing ER activity and suppressing ferroptosis, demonstrating that ZNF570 may act as a promising therapeutic target for reversing tamoxifen resistance in ER + BC. - Source: PubMed
Publication date: 2026/03/20
Ren YunZhang JindanDuan MingtingZhao ZiweiGuo RuqiXu JianzhongWang YanhongJia Hongyan - DNA methylation has started a recent revolution in genomics biology by identifying key biomarkers for multiple cancers, including oral squamous cell carcinoma (OSCC), the most common head and neck squamous cell carcinoma. - Source: PubMed
Publication date: 2017/08/24
Shen SipengWang GuanrongShi QianwenZhang RuyangZhao YangWei YongyueChen FengChristiani David C - Chromosome territories assume non-random positions in the interphase nucleus with gene-rich chromosomes localized toward the nuclear interior and gene-poor chromosome territories toward the nuclear periphery. Lamins are intermediate filament proteins of the inner nuclear membrane required for the maintenance of nuclear structure and function. Here, we show using whole-genome expression profiling that Lamin A/C or Lamin B2 depletion in an otherwise diploid colorectal cancer cell line (DLD1) deregulates transcript levels from specific chromosomes. Further, three-dimensional fluorescence in situ hybridization (3D-FISH) analyses of a subset of these transcriptionally deregulated chromosome territories revealed that the diploid chromosome territories in Lamin-depleted cells largely maintain conserved positions in the interphase nucleus in a gene-density-dependent manner. In addition, chromosomal aneuploidies were induced in ~25 % of Lamin A/C or Lamin B2-depleted cells. Sub-populations of these aneuploid cells consistently showed a mislocalization of the gene-rich aneuploid chromosome 19 territory toward the nuclear periphery, while gene-poor aneuploid chromosome 18 territory was mislocalized toward the nuclear interior predominantly upon Lamin B2 than Lamin A/C depletion. In addition, a candidate gene locus ZNF570 (Chr.19q13.12) significantly overexpressed upon Lamin B2 depletion was remarkably repositioned away from the nuclear lamina. Taken together, our studies strongly implicate an overarching role for Lamin B2 in the maintenance of nuclear architecture since loss of Lamin B2 relieves the spatial positional constraints required for maintaining conserved localization of aneuploid chromosome territories in the interphase nucleus. - Source: PubMed
Publication date: 2016/02/27
Ranade DevikaKoul ShivsmritiThompson JoycePrasad Kumar BrajeshSengupta Kundan