ArticleNeoplasia (New York, N.Y.)2014
Deletion of atbf1/zfhx3 in mouse prostate causes neoplastic lesions, likely by attenuation of membrane and secretory proteins and multiple signaling pathways.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Recurrent mechanisms of biallelic epigenetic inactivation reveal new putative tumour suppressor genes in prostate cancer.Nature communications · 2026Article
- Cell villages and Dirichlet modeling map human cell fitness genetics.bioRxiv : the preprint server for biology · 2025Article
- ZFHX3 is integral to androgen/AR signaling involving protein association with AR in prostate cancer cells.Scientific reports · 2025Article
- Evaluation of Potential Roles of Zinc Finger Homeobox 3 (Zfhx3) Expressed in Chondrocytes and Osteoblasts on Skeletal Growth in Mice.Calcified tissue international · 2024Article
- Somatic mutational landscape across Indian breast cancer cases by whole exome sequencing.Scientific reports · 2024Article
- ZFHX3 acts as a tumor suppressor in prostate cancer by targeting FTO-mediated mCell death discovery · 2024Article
- Signal Crosstalk and the Role of Estrogen Receptor beta (ERβ) in Prostate Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2022Review
- AR imposes different effects on ZFHX3 transcription depending on androgen status in prostate cancer cells.Journal of cellular and molecular medicine · 2022Article
- Sodium bicarbonate transporter NBCe1 regulates proliferation and viability of human prostate cancer cells LNCaP and PC3.Oncology reports · 2021Article
- Circulating Tumor Cell Genomic Evolution and Hormone Therapy Outcomes in Men with Metastatic Castration-Resistant Prostate Cancer.Molecular cancer research : MCR · 2021Article
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- Genomic Profiling of Prostate Cancers from Men with African and European Ancestry.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- The transcription factor ZFHX3 is crucial for the angiogenic function of hypoxia-inducible factor 1α in liver cancer cells.The Journal of biological chemistry · 2020Article
- SUMOylation of the transcription factor ZFHX3 at Lys-2806 requires SAE1, UBC9, and PIAS2 and enhances its stability and function in cell proliferation.The Journal of biological chemistry · 2020Article
- zfh2 controls progenitor cell activation and differentiation in the adult Drosophila intestinal absorptive lineage.PLoS genetics · 2019Article
- ZFHX3 is indispensable for ERβ to inhibit cell proliferation via MYC downregulation in prostate cancer cells.Oncogenesis · 2019Article
- Article
- Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.Nature genetics · 2018Article
- Zinc Finger Homeodomain Factor Zfhx3 Is Essential for Mammary Lactogenic Differentiation by Maintaining Prolactin Signaling Activity.The Journal of biological chemistry · 2016Article
- Identification of Drosophila Zfh2 as a Mediator of Hypercapnic Immune Regulation by a Genome-Wide RNA Interference Screen.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The ATBF1/ZFHX3 gene at 16q22 is the second most frequently mutated gene in human prostate cancer and has reduced expression or mislocalization in several types of human tumors. Nonetheless, the hypothesis that ATBF1 has a tumor suppressor function in prostate cancer has not been tested. In this study, we examined the role of ATBF1 in prostatic carcinogenesis by specifically deleting Atbf1 in mouse prostatic epithelial cells. We also examined the effect of Atbf1 deletion on gene expression and signaling pathways in mouse prostates. Histopathologic analyses showed that Atbf1 deficiency caused hyperplasia and mouse prostatic intraepithelial neoplasia (mPIN) primarily in the dorsal prostate but also in other lobes. Hemizygous deletion of Atbf1 also increased the development of hyperplasia and mPIN, indicating a haploinsufficiency of Atbf1. The mPIN lesions expressed luminal cell markers and harbored molecular changes similar to those in human PIN and prostate cancer, including weaker expression of basal cell marker cytokeratin 5 (Ck5), cell adhesion protein E-cadherin, and the smooth muscle layer marker Sma; elevated expression of the oncoproteins phospho-Erk1/2, phospho-Akt and Muc1; and aberrant protein glycosylation. Gene expression profiling revealed a large number of genes that were dysregulated by Atbf1 deletion, particularly those that encode for secretory and cell membrane proteins. The four signaling networks that were most affected by Atbf1 deletion included those centered on Erk1/2 and IGF1, Akt and FSH, NF-κB and progesterone and β-estradiol. These findings provide in vivo evidence that ATBF1 is a tumor suppressor in the prostate, suggest that loss of Atbf1 contributes to tumorigenesis by dysregulating membrane and secretory proteins and multiple signaling pathways, and provide a new animal model for prostate cancer.
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