ArticleOncogene2004
Krüppel-like factor 5 mediates the transforming activity of oncogenic H-Ras.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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.
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Who cites it
84 citing papers in PubMed, 137 citations in OpenAlex.
- KLF family of proteins in gastrointestinal tumors (Review).Oncology letters · 2026Review
- KLF5 Shapes Developing Respiratory Tubules by Inhibiting Actin Asymmetry in Epithelial Cells.American journal of respiratory cell and molecular biology · 2025Article
- Krüppel-like Factor 5 Plays an Important Role in the Pathogenesis of Chronic Pancreatitis.Cancers · 2023Article
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- Review
- Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022Review
- Krüppel-like factor 5 is upregulated and induces cell proliferation in endometrial cancer.Oncology letters · 2021Article
- KLF5-mediated Eppk1 expression promotes cell proliferation in cervical cancer via the p38 signaling pathway.BMC cancer · 2021Article
- A novel mechanism driving poor-prognostic gastric cancer: overexpression of the transcription factor Krüppel-like factor 16 promotes growth and metastasis of gastric cancer through regulating the Notch pathway.American journal of cancer research · 2021Article
- High expression of Krüppel-like factor 5 is associated with poor prognosis in patients with colorectal cancer.Cancer science · 2020Article
- Krüppel-like Factor 5 Regulates Stemness, Lineage Specification, and Regeneration of Intestinal Epithelial Stem Cells.Cellular and molecular gastroenterology and hepatology · 2020Article
- Network analysis ofCancer cell international · 2020Article
- Causal Inference Engine: a platform for directional gene set enrichment analysis and inference of active transcriptional regulators.Nucleic acids research · 2019Article
- Krüppel-like Factor 5 Promotes Sonic Hedgehog Signaling and Neoplasia in Barrett's Esophagus and Esophageal Adenocarcinoma.Translational oncology · 2019Article
- The Novel Small-Molecule SR18662 Efficiently Inhibits the Growth of Colorectal CancerMolecular cancer therapeutics · 2019Article
- The Krüppel-like factor (KLF5) as a predictive biomarker in preoperative chemoradiation therapy for rectal cancer.Annals of surgical treatment and research · 2019Article
- Overexpression of KLF5 is associated with poor survival and G1/S progression in pancreatic cancer.Aging · 2019Article
- Clinical Significance of Lysophosphatidic Acid Receptor-2 (LPA2) and Krüppel-Like Factor 5 (KLF5) Protein Expression Detected by Tissue Microarray in Gastric Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Article
- The transcription factor Klf5 is essential for intrahepatic biliary epithelial tissue remodeling after cholestatic liver injury.The Journal of biological chemistry · 2018Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies indicate that Krüppel-like factor 5 (KLF5), also known as intestinal-enriched Krüppel-like factor (IKLF), is a positive regulator of cell proliferation and gives rise to a transformed phenotype when overexpressed. Here we demonstrate that levels of KLF5 transcript and protein are significantly elevated in oncogenic H-Ras-transformed NIH3T3 cells. These cells display an accelerated rate of proliferation in both serum-containing and serum-deprived media and form anchorage-independent colonies in soft agar assays. H-Ras-transformed cells also contain elevated mitogen-activated protein kinase (MAPK) activity. When treated with inhibitors of MEK (MAPK kinase), H-Ras-transformed cells lose their growth advantage and no longer form colonies. Significantly, levels of KLF5 transcript and protein are substantially reduced in H-Ras-transformed cells treated with MEK inhibitors. Moreover, inhibition of KLF5 expression in H-Ras-transformed cells with KLF5-specific small interfering RNA (siRNA) leads to a decreased rate of proliferation and a significant reduction in colony formation. H-Ras-transformed cells also contain elevated levels of Egr1 that are diminished by MEK inhibitors. Inhibition of Egr1 by siRNA results in a reduced level of KLF5, indicating that Egr1 mediates the inductive action of MAPK on KLF5. Lastly, KLF5 activates expression of cyclin D1. These findings indicate that the increased expression of KLF5 in H-Ras-transformed cells is secondary to increased MAPK activity from H-Ras overexpression and that the elevated level of KLF5 is in part responsible for the proproliferative and transforming activities of oncogenic H-Ras.
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What OpenQuestion holds
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.