ArticleOncotarget2016
Loss of ZNF32 augments the regeneration of nervous lateral line system through negative regulation of SOX2 transcription.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- ZNF32 histidine 179 and 183 single-site and double-site mutations promote nuclear speckle formation but differentially regulate the proliferation of breast cancer cells.Frontiers in cell and developmental biology · 2025Article
- Transcriptomic response of overexpression ZNF32 in breast cancer cells.Scientific reports · 2024Article
- ZNF32 promotes the self-renewal of colorectal cancer cells by regulating the LEPR-STAT3 signaling pathway.Cell death & disease · 2022Article
- Article
- Zinc finger protein 32 promotes breast cancer stem cell-like properties through directly promoting GPER transcription.Cell death & disease · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human zinc finger protein 32 (ZNF32) is a Cys2-His2 zinc-finger transcription factor that plays an important role in cell fate, yet much of its function remains unknown. Here, we reveal that the zebrafish ZNF32 homologue zfZNF32 is expressed in the nervous system, particularly in the lateral line system. ZfZNF32 knock-out zebrafish (zfZNF-/-) were generated using the CRISPR-associated protein 9 system. We found that the regenerative capacity of the lateral line system was increased in zfZNF-/- upon hair cell damage compared with the wild type. Moreover, SOX2 was essential for the zfZNF32-dependent modulation of lateral line system regeneration. Mechanistic studies showed that ZNF32 suppressed SOX2 transcription by directly binding to a consensus sequence (5'-gcattt-3') in the SOX2 promoter. In addition, ZNF32 localizes to the nucleus, and we have identified that amino acids 1-169 (Aa 1-169) and each of three independent nuclear localization signals (NLSs) in ZNF32 are indispensable for ZNF32 nuclear trafficking. Mutating the NLSs disrupted the inhibitory effect of ZNF32 in SOX2 expression, highlighting the critical role of the NLSs in ZNF32 function. Our findings reveal a pivotal role for ZNF32 function in SOX2 expression and regeneration regulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.