ArticleThe American journal of pathology2010
Kruppel-like factor 5 is not required for K-RasG12D lung tumorigenesis, but represses ABCG2 expression and is associated with better disease-specific survival.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Comprehensive Analysis of Macrophage Dynamics, CCBE1, and Their Implications in Colorectal Cancer Microenvironment: Insights Into Tumor Progression and Therapeutic Opportunities.Genetics research · 2026Article
- KLF5-regulated ZDHHC8 reduces chemosensitivity in high-grade serous ovarian cancer through β-catenin signaling.Scientific reports · 2025Article
- KLF5 Shapes Developing Respiratory Tubules by Inhibiting Actin Asymmetry in Epithelial Cells.American journal of respiratory cell and molecular biology · 2025Article
- Identification of a novel tRNA-derived small RNA fragment, tRF-16-2YU04DE, with the potential of inhibiting endometrial cancer progression.Medical oncology (Northwood, London, England) · 2025Article
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- Krüppel-like factor 5 is upregulated and induces cell proliferation in endometrial cancer.Oncology letters · 2021Article
- KLF5 Is Activated by Gene Amplification in Gastric Cancer and Is Essential for Gastric Cell Proliferation.Cells · 2021Article
- Knockdown of KLF5 suppresses hypoxia-induced resistance to cisplatin in NSCLC cells by regulating HIF-1α-dependent glycolysis through inactivation of the PI3K/Akt/mTOR pathway.Journal of translational medicine · 2018Article
- KLF15 Inhibits Cell Proliferation in Gastric Cancer Cells via Up-Regulating CDKN1A/p21 and CDKN1C/p57 Expression.Digestive diseases and sciences · 2017Article
- Role of Krüppel-like factors in cancer stem cells.Journal of physiology and biochemistry · 2015Review
- Krüppel-like factors in hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
K-RAS mutations are found in approximately 30% of lung cancers. The transcription factor Krüppel-like Factor 5 (KLF5) has been shown to mediate cellular transformation signaling events downstream of oncogenic RAS in other cancers, but a role for KLF5 in lung tumorigenesis has not been defined. We show here that knockdown of KLF5 expression significantly decreased anchorage-independent growth, but did not affect proliferation of human lung adenocarcinoma cells. Moreover, Klf5 is not required for lung tumor formation in an inducible oncogenic K-Ras(G12D) mouse model of lung tumorigenesis, and non-small cell lung cancer patients expressing high levels of KLF5 (21/258) have a significantly better disease-specific survival than those with intermediate to no KLF5 expression. Further, KLF5 knockdown in K-RAS-mutant human lung cancer cells resulted in a fivefold increase in ATP-binding cassette, subfamily G (WHITE), member 2 (ABCG2), an anthracycline drug transporter, which lead to significantly increased resistance to doxorubicin treatment, a chemotherapeutic agent clinically used to treat lung cancer. In summary, while KLF5 is not required for oncogenic mutant K-Ras-induced lung tumorigenesis, KLF5 regulation of ABCG2 expression may be important for chemotherapeutic resistance and patient survival.
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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.