ArticleThe American journal of pathology2012
KLF6 loss of function in human prostate cancer progression is implicated in resistance to androgen deprivation.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Multi-Omics Analysis of the Anoikis GeneBiomedicines · 2025Article
- Prediction of Potential Biomarkers in Early-Stage Nasopharyngeal Carcinoma Based on Platelet RNA Sequencing.Molecular biotechnology · 2023Article
- LncRNAs in the Regulation of Genes and Signaling Pathways through miRNA-Mediated and Other Mechanisms in Clear Cell Renal Cell Carcinoma.International journal of molecular sciences · 2021Review
- Comprehensive analysis of alternative splicing profiling reveals novel events associated with prognosis and the infiltration of immune cells in prostate cancer.Translational andrology and urology · 2021Article
- Meiotic nuclear divisions 1 (MND1) fuels cell cycle progression by activating a KLF6/E2F1 positive feedback loop in lung adenocarcinoma.Cancer communications (London, England) · 2021Article
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
- Alternative splicing in prostate cancer.Nature reviews. Clinical oncology · 2018Review
- Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.Wiley interdisciplinary reviews. RNA · 2018Review
- Targeting Splicing in Prostate Cancer.International journal of molecular sciences · 2018Review
- The molecular biology of prostate cancer: current understanding and clinical implications.Prostate cancer and prostatic diseases · 2018Review
- Genetic heterogeneity of primary lesion and metastasis in small intestine neuroendocrine tumors.Scientific reports · 2018Article
- Overexpression of the Oncogenic Variant (KLF6-SV1) in Young NPC Patients and Correlation with Lack of E-Cadherin.Analytical cellular pathology (Amsterdam) · 2018Article
- c-Myc Antagonises the Transcriptional Activity of the Androgen Receptor in Prostate Cancer Affecting Key Gene Networks.EBioMedicine · 2017Article
- The Krüppel-like factors in female reproductive system pathologies.Journal of molecular endocrinology · 2015Review
- Insulin-like growth factor receptor-1 (IGF-IR) as a target for prostate cancer therapy.Cancer metastasis reviews · 2014Review
- Identification of miRNAs that specifically target tumor suppressive KLF6-FL rather than oncogenic KLF6-SV1 isoform.RNA biology · 2014Article
- Krüppel-like factors in cancer.Nature reviews. Cancer · 2013Review
- Molecular pathology of prostate cancer revealed by next-generation sequencing: opportunities for genome-based personalized therapy.Current opinion in urology · 2013Review
- Effects of Kruppel-like factor 6 on osteosarcoma cell biological behavior.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Alternative splicing programs in prostate cancer.International journal of cell biology · 2013Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 3 countries.
Funding
Abstract
Inactivation of the transcription factor/tumor suppressor Krüppel-like factor 6 (KLF6) has been described in prostate cancer (PC). This study investigated the prevalence and significance of KLF6 exon 2 mutations and splice variants (SVs) in different stages of human PC progression. By using laser-capture microdissection and recombinant clone isolation of DNA sequences to enhance sensitivity, base changes were found in 20 (24.7%) of 81 PC tissues versus 1 (4%) of 25 normal prostate tissues (P = 0.02). Of 26 base changes, 54% produced nonsynonymous mutations. Only three mutations had driver characteristics (PCs, 4%; NPs, 0%). By using microdissection of fresh-frozen tissues and recombinant isolation of RNA sequences, SVs were found in 39 (75%) of 52 PCs and in 10 (45%) of 22 NPs (P = 0.01). Sixteen different SVs, including 13 unique SVs, were identified that used cryptic splicing sites and encoded nonfunctional KLF6 proteins. PCs that had survived hormone (androgen)-deprivation therapy (n = 21) had a significantly higher (P < 0.05) incidence, number, and expression level of nonfunctional SVs than either NPs (n = 22) or hormone-naïve PCs (n = 25). Forced expression of nonfunctional SVs conferred a survival advantage of androgen-dependent LNCaP cells under castration-simulated culture conditions. Together, these data suggest that decreased availability of functional KLF6 contributes to clinical PC progression. This decrease arises infrequently by somatic mutation and more commonly by the acquisition of SVs that provide a survival advantage under castrate conditions, enabling resistance to hormone therapy.
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