ArticleThe Journal of biological chemistry2012
Novel insight into KLF4 proteolytic regulation in estrogen receptor signaling and breast carcinogenesis.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Pooled it
- Prognostic Significance of miR-145, NANOG, OCT4, and KLF4 in Triple-Negative Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Regional and Sexual Dimorphism in Murine Skeletal Responses to Osteocytic HIF Pathway Modulation.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Gene expression profiling of KLF4 and KLF5 in visceral adipose tissue of obese women: insights into adipogenic and metabolic regulation.Lipids in health and disease · 2025Article
- Metabolic Switch in Endocrine Resistant Estrogen Receptor Positive Breast Cancer.bioRxiv : the preprint server for biology · 2024Article
- Article
- Pharmacological suppression of the OTUD4/CD73 proteolytic axis revives antitumor immunity against immune-suppressive breast cancers.The Journal of clinical investigation · 2024Article
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- Proteolytic regulation of CD73 by TRIM21 orchestrates tumor immunogenicity.Science advances · 2023Article
- Transcription Factors: The Fulcrum Between Cell Development and Carcinogenesis.Frontiers in oncology · 2021Review
- Review
- Regulation of KLF4 by posttranslational modification circuitry in endocrine resistance.Cellular signalling · 2020Article
- The Clinical Relevance and Function of Krüppel-Like Factor 16 in Breast Cancer.Cancer management and research · 2020Article
- KLF4 protein stability regulated by interaction with pluripotency transcription factors overrides transcriptional control.Genes & development · 2019Article
- Emerging role of DUBs in tumor metastasis and apoptosis: Therapeutic implication.Pharmacology & therapeutics · 2017Review
- FBXO32 suppresses breast cancer tumorigenesis through targeting KLF4 to proteasomal degradation.Oncogene · 2017Article
- Transcriptional landscape of the human cell cycle.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Regulation of XIAP Turnover Reveals a Role for USP11 in Promotion of Tumorigenesis.EBioMedicine · 2017Article
- Kruppel-like factor4 regulatesJCI insight · 2017Article
- Interplay between arginine methylation and ubiquitylation regulates KLF4-mediated genome stability and carcinogenesis.Nature communications · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Krüppel-like factor 4 (KLF4), a zinc finger-containing transcriptional factor, is a pivotal regulator of cellular fate. KLF4 has attracted considerable attention for its opposing effect in carcinogenesis as tumor suppressor (e.g. colorectal cancer) or oncoprotein (e.g. breast cancer), depending on tissue context, with the underlying mechanism remaining largely unknown. Here we report that KLF4 mediates estrogen signaling in breast cancer formation. Accumulation of KLF4 by inhibiting its turnover triggers estrogen-induced transactivation. We identified Von Hippel-Lindau, pVHL, as the protein that governs KLF4 turnover in breast cancer cells and demonstrated that estrogen-induced down-regulation of pVHL facilitates accumulation of KLF4. We provide mechanistic insights into KLF4 steady-state degradation as well as its elevation in the presence of estrogen and show that elevated levels of pVHL or depletion of KLF4 attenuates the estrogen-induced transactivation and cell growth. Finally, immunohistochemical staining revealed reduced concentration of pVHL and accumulation of KLF4 in breast cancer tissues. We thus propose that suppression of pVHL in response to estrogen signaling results in elevation of KLF4, which mediates estrogen-induced mitogenic effect.
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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.