ArticleNeoplasia (New York, N.Y.)2014
Klf5 deletion promotes Pten deletion-initiated luminal-type mouse prostate tumors through multiple oncogenic signaling pathways.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Recurrent mechanisms of biallelic epigenetic inactivation reveal new putative tumour suppressor genes in prostate cancer.Nature communications · 2026Article
- Cellular cartography reveals mouse prostate organization and determinants of castration resistance.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comparative transcriptomics reveals a mixed basal, club, and hillock epithelial cell identity in castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Participation of Krüppel-like Factors in Atherogenesis.Metabolites · 2023Review
- Opposing transcriptional programs of KLF5 and AR emerge during therapy for advanced prostate cancer.Nature communications · 2021Article
- miR-9 modulates and predicts the response to radiotherapy and EGFR inhibition in HNSCC.EMBO molecular medicine · 2021Article
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- KLF5 Is Activated by Gene Amplification in Gastric Cancer and Is Essential for Gastric Cell Proliferation.Cells · 2021Article
- MiR-203 Targets to the 3'-UTR of SLUG to Suppress Cerebral Infarction-Induced Endothelial Cell Growth and Motility.Evidence-based complementary and alternative medicine : eCAM · 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
- 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
- Upregulation of MicroRNA-21 promotes tumorigenesis of prostate cancer cells by targeting KLF5.Cancer biology & therapy · 2019Article
- KLF5 downregulation desensitizes castration-resistant prostate cancer cells to docetaxel by increasing BECN1 expression and inducing cell autophagy.Theranostics · 2019Article
- Molecular Evolution of Early-Onset Prostate Cancer Identifies Molecular Risk Markers and Clinical Trajectories.Cancer cell · 2018Article
- Characterization and Evidence of the miR-888 Cluster as a Novel Cancer Network in Prostate.Molecular cancer research : MCR · 2018Article
- KLF5 promotes apoptosis induced by phorbol ester as an effector of the autocrine factor TNFα in LNCaP prostate cancer cells.Oncology letters · 2017Article
- DNMT1-maintained hypermethylation of Krüppel-like factor 5 involves in the progression of clear cell renal cell carcinoma.Cell death & disease · 2017Article
- The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis.Frontiers in molecular neuroscience · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Krüppel-like factor 5 (KLF5) regulates multiple biologic processes. Its function in tumorigenesis appears contradictory though, showing both tumor suppressor and tumor promoting activities. In this study, we examined whether and how Klf5 functions in prostatic tumorigenesis using mice with prostate-specific deletion of Klf5 and phosphatase and tensin homolog (Pten), both of which are frequently inactivated in human prostate cancer. Histologic analysis demonstrated that when one Pten allele was deleted, which causes mouse prostatic intraepithelial neoplasia (mPIN), Klf5 deletion accelerated the emergence and progression of mPIN. When both Pten alleles were deleted, which causes prostate cancer, Klf5 deletion promoted tumor growth, increased cell proliferation, and caused more severe morphologic and molecular alterations. Homozygous deletion of Klf5 was more effective than hemizygous deletion. Unexpectedly, while Pten deletion alone expanded basal cell population in a tumor as reported, Klf5 deletion in the Pten-null background clearly reduced basal cell population while expanding luminal cell population. Global gene expression profiling, pathway analysis, and experimental validation indicate that multiple mechanisms could mediate the tumor-promoting effect of Klf5 deletion, including the up-regulation of epidermal growth factor and its downstream signaling molecules AKT and ERK and the inactivation of the p15 cell cycle inhibitor. KLF5 also appears to cooperate with several transcription factors, including CREB1, Sp1, Myc, ER and AR, to regulate gene expression. These findings validate the tumor suppressor function of KLF5. They also yield a mouse model that shares two common genetic alterations with human prostate cancer-mutation/deletion of Pten and deletion of Klf5.
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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.