ArticleCancers2011
Forced Expression of ZNF143 Restrains Cancer Cell Growth.
Article in Cancers, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Integrated multi-cohort transcriptional meta-analysis of neurodegenerative diseases.Acta neuropathologica communications · 2014Pooled it
- Zinc Finger Protein 143 Bidirectionally Regulates the Proliferation of Hepatocytes and Hepatocellular Carcinoma Cells via c-Myc.Cell biochemistry and function · 2026Article
- Putative looping factor ZNF143/ZFP143 is an essential transcriptional regulator with no looping function.Molecular cell · 2025Article
- The role of ZNF143 overexpression in rat liver cell proliferation.BMC genomics · 2022Article
- ZNF143 in Chromatin Looping and Gene Regulation.Frontiers in genetics · 2020Review
- Loss of zinc-finger protein 143 contributes to tumour progression by interleukin-8-CXCR axis in colon cancer.Journal of cellular and molecular medicine · 2019Article
- Article
- Expression of zinc finger transcription factors (ZNF143 and ZNF281) in serous borderline ovarian tumors and low-grade ovarian cancers.Journal of ovarian research · 2019Article
- Zinc finger protein 143 expression is closely related to tumor malignancy via regulating cell motility in breast cancer.BMB reports · 2017Article
- Statin and Bisphosphonate Induce Starvation in Fast-Growing Cancer Cell Lines.International journal of molecular sciences · 2017Article
- YPC-21661 and YPC-22026, novel small molecules, inhibit ZNF143 activity in vitro and in vivo.Cancer science · 2017Article
- ZNF143 enhances metastasis of gastric cancer by promoting the process of EMT through PI3K/AKT signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Strong expression of polypeptide N-acetylgalactosaminyltransferase 3 independently predicts shortened disease-free survival in patients with early stage oral squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Mitochondrial Transcription Factor A and Mitochondrial Genome as Molecular Targets for Cisplatin-Based Cancer Chemotherapy.International journal of molecular sciences · 2015Review
- Transcription factor abundance controlled by an auto-regulatory mechanism involving a transcription start site switch.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that the transcription factor Zinc Finger Protein 143 (ZNF143) regulates the expression of genes associated with cell cycle and cell division, and that downregulation of ZNF143 induces cell cycle arrest at G2/M. To assess the function of ZNF143 expression in the cell cycle, we established two cells with forced expression of ZNF143 derived from PC3 prostate cancer cell lines. These cell lines overexpress genes associated with cell cycle and cell division, such as polo-like kinase 1 (PLK1), aurora kinase B (AURKB) and some minichromosome maintenance complex components (MCM). However, the doubling time of cells with forced expression of ZNF143 was approximately twice as long as its control counterpart cell line. Analysis following serum starvation and re-seeding showed that PC3 cells were synchronized at G1 in the cell cycle. Also, ZNF143 expression fluctuated, and was at its lowest level in G2/M. However, PC3 cells with forced expression of ZNF143 synchronized at G2/M, and showed lack of cell cycle-dependent fluctuation of nuclear expression of MCM proteins. Furthermore, G2/M population of both cisplatin-resistant PCDP6 cells over-expressing ZNF143 (derived from PC3 cells) and cells with forced expression of ZNF143 was significantly higher than that of each counterpart, and the doubling time of PCDP6 cells is about 2.5 times longer than that of PC3 cells. These data suggested that fluctuations in ZNF143 expression are required both for gene expression associated with cell cycle and for cell division.
Identifiers
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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.