ArticleThe Journal of biological chemistry2013
Kruppel-like factor 5 transcription factor promotes microsomal prostaglandin E2 synthase 1 gene transcription in breast cancer.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- KLF9 Inhibits Brain Metastasis of Non-Small Cell Lung Cancer by Regulating Ceramide Synthase 1 Synthesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Positive Feedback Regulation between KLF5 and XPO1 Promotes Cell Cycle Progression of Basal like Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- BRD4-specific PROTAC inhibits basal-like breast cancer partially through downregulating KLF5 expression.Oncogene · 2024Article
- A novel role of master regulator transcription factor in anti-tumor immunity and cancer immunotherapy.Theranostics · 2023Article
- KLF5 inhibition potentiates anti-PD1 efficacy by enhancing CD8Theranostics · 2023Article
- Review
- YB-1 is a positive regulator of KLF5 transcription factor in basal-like breast cancer.Cell death and differentiation · 2022Article
- Expression and Prognosis Value of the KLF Family Members in Colorectal Cancer.Journal of oncology · 2022Article
- Histone Deacetylase Inhibitors (HDACi) Promote KLF5 Ubiquitination and Degradation in Basal-like Breast Cancer.International journal of biological sciences · 2022Article
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- Targeted eicosanoids profiling reveals a prostaglandin reprogramming in breast Cancer by microRNA-155.Journal of experimental & clinical cancer research : CR · 2021Article
- Low Salt Delivery Triggers Autocrine Release of Prostaglandin E2 From the Aldosterone-Sensitive Distal Nephron in Familial Hyperkalemic Hypertension Mice.Frontiers in physiology · 2021Article
- KLF5 regulates epithelial-mesenchymal transition of liver cancer cells in the context of p53 loss through miR-192 targeting of ZEB2.Cell adhesion & migration · 2020Article
- USP3 promotes breast cancer cell proliferation by deubiquitinating KLF5.The Journal of biological chemistry · 2019Article
- Overexpression of KLF5 is associated with poor survival and G1/S progression in pancreatic cancer.Aging · 2019Article
- Stress and drug resistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2019Review
- Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers.International journal of biological sciences · 2019Article
- The roles of TNFAIP2 in cancers and infectious diseases.Journal of cellular and molecular medicine · 2018Review
- 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
- Down-regulation of KLF5 in cancer-associated fibroblasts inhibit gastric cancer cells progression by CCL5/CCR5 axis.Cancer biology & therapy · 2017Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The KLF5 (Krüppel-like factor 5) transcription factor is specifically expressed in a subset of estrogen receptor α-negative breast cancers. Although KLF5 promotes breast cancer cell cycle progression, survival, and tumorigenesis, the mechanism by which KLF5 promotes breast cancer is still not entirely understood. Here, we demonstrate that mPGES1, encoding microsomal prostaglandin E2 synthase 1 (mPGES1), is a KLF5 direct downstream target gene. KLF5 overexpression or knockdown positively altered the levels of mPGES1 mRNA and protein in multiple breast cell lines. 12-O-Tetradecanoylphorbol-13-acetate induced the expression of both KLF5 and mPGES1 in dosage- and time-dependent manners. The induction of KLF5 was essential for 12-O-tetradecanoylphorbol-13-acetate to induce mPGES1 expression. Additionally, KLF5 bound to the mPGES1 gene proximal promoter and activated its transcription. Both KLF5 and mPGES1 promoted prostaglandin E2 production; regulated p21, p27, and Survivin downstream gene expression; and likewise stimulated cell proliferation. Overexpression of mPGES1 partially rescued the KLF5 knockdown-induced downstream gene expression changes and growth arrest in MCF10A cells. Finally, we demonstrate that the expression of mPGES1 was positively correlated with the estrogen receptor α/progesterone receptor/HER2 triple-negative status. These findings suggest that mPGES1 is a target gene of KLF5, making it a new biomarker and a potential therapeutic target for triple-negative breast cancers.
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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.