ArticleInternational journal of cancer2015
Interruption of KLF5 acetylation converts its function from tumor suppressor to tumor promoter in prostate cancer cells.
Article in International journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Computational screening and molecular dynamics of natural compounds targeting the SH2 domain of STAT3: a multitarget approach using network pharmacology.Molecular diversity · 2025Article
- Dissecting the role of KLF5: from tumor progression to immune interactions with emphasis on glioma and bladder cancer.Frontiers in immunology · 2025Article
- Multi-faceted regulation of CREB family transcription factors.Frontiers in molecular neuroscience · 2024Review
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- Nitazoxanide inhibits acetylated KLF5-induced bone metastasis by modulating KLF5 function in prostate cancer.BMC medicine · 2023Article
- KLF5 inhibition potentiates anti-PD1 efficacy by enhancing CD8Theranostics · 2023Article
- Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022Review
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer.Nature communications · 2021Article
- Roles of Krüppel-like factor 5 in kidney disease.Journal of cellular and molecular medicine · 2021Review
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
- Predicting 3D Structure, Cross Talks, and Prognostic Significance ofFrontiers in oncology · 2021Article
- KLF5 Is Crucial for Androgen-AR Signaling to Transactivate Genes and Promote Cell Proliferation in Prostate Cancer Cells.Cancers · 2020Article
- Klf5 acetylation regulates luminal differentiation of basal progenitors in prostate development and regeneration.Nature communications · 2020Article
- Network analysis ofCancer cell international · 2020Article
- TGF-β causes Docetaxel resistance in Prostate Cancer via the induction of Bcl-2 by acetylated KLF5 and Protein Stabilization.Theranostics · 2020Article
- Article
- CINP is a novel cofactor of KLF5 required for its role in the promotion of cell proliferation, survival and tumor growth.International journal of cancer · 2019Article
- HIV-associated sensory polyneuropathy and neuronal injury are associated with miRNA-455-3p induction.JCI insight · 2018Article
- ZNF121 interacts with ZBRK1 and BRCA1 to regulate their target genes in mammary epithelial cells.FEBS open bio · 2018Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
KLF5 possesses both tumor suppressing and tumor promoting activities, though the mechanism controlling these opposing functions is unknown. In cultured noncancerous epithelial cells, KLF5 converts from proproliferative to antiproliferative activity upon TGFβ-induced acetylation, which sequentially alters the KLF5 transcriptional complex and the expression of genes such as p15 and MYC. In this study, we tested whether the acetylation status of KLF5 also determines its opposing functions in tumorigenesis using the PC-3 and DU 145 prostate cancer cell lines, whose proliferation is inhibited by TGFβ. KLF5 inhibited the proliferation of these cancer cells, and the inhibition was dependent on KLF5 acetylation. MYC and p15 showed the same patterns of expression change found in noncancerous cells. In nude mice, KLF5 also suppressed tumor growth in an acetylation-dependent manner. Furthermore, deacetylation switched KLF5 to tumor promoting activity, and blocking TGFβ signaling attenuated the tumor suppressor activity of KLF5. RNA sequencing and comprehensive data analysis suggest that multiple molecules, including RELA, p53, CREB1, MYC, JUN, ER, AR and SP1, mediate the opposing functions of AcKLF5 and unAcKLF5. These results provide novel insights into the mechanism by which KLF5 switches from antitumorigenic to protumorigenic function and also suggest the roles of AcKLF5 and unAcKLF5, respectively, in the tumor suppressing and tumor promoting functions of TGFβ.
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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.