ArticleOncogenesis2018
SUMOylation modulates FOXK2-mediated paclitaxel sensitivity in breast cancer cells.
Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- AKT Phosphorylation of FOXK2 at Ser398 Impacts Breast Cancer Cell Growth and Viability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- FOXK2/SH2D3A axis recruits EGFR to drive papillary thyroid cancer progression and confers sensitivity to EGFR inhibition.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
- The role of FOXK2-FBXO32 in breast cancer tumorigenesis: Insights into ribosome-associated pathways.Thoracic cancer · 2025Article
- Conserved linear motif within the immediate early protein ORF45 promotes its engagement with KSHV lytic cycle-promoting forkhead transcription factors, FOXK1 and FOXK2.Journal of virology · 2024Article
- FOXK2 targeting by the SCF-E3 ligase subunit FBXO24 for ubiquitin mediated degradation modulates mitochondrial respiration.The Journal of biological chemistry · 2024Article
- Phosphorylation of FOXK2 at Thr13 and Ser30 by PDK2 sustains glycolysis through a positive feedback manner in ovarian cancer.Oncogene · 2024Article
- Role and regulation of FOXO3a: new insights into breast cancer therapy.Frontiers in pharmacology · 2024Review
- Emerging roles of FOXK2 in cancers and metabolic disorders.Frontiers in oncology · 2024Review
- Exploring the Role of Unconventional Post-Translational Modifications in Cancer Diagnostics and Therapy.Current protein & peptide science · 2024Review
- FOXK2 transcription factor and its roles in tumorigenesis (Review).Oncology letters · 2022Review
- Regulation and roles of FOXK2 in cancer.Frontiers in oncology · 2022Review
- The deacetylation of Foxk2 by Sirt1 reduces chemosensitivity to cisplatin.Journal of cellular and molecular medicine · 2022Article
- FOXK2 transcriptionally activating VEGFA induces apatinib resistance in anaplastic thyroid cancer through VEGFA/VEGFR1 pathway.Oncogene · 2021Article
- SUMO4 small interfering RNA attenuates invasion and migration via the JAK2/STAT3 pathway in non-small cell lung cancer cells.Oncology letters · 2020Article
- Brahma Related Gene 1 (Brg1) Regulates Cellular Cholesterol Synthesis by Acting as a Co-factor for SREBP2.Frontiers in cell and developmental biology · 2020Article
- Prognostic Value of the FOXK Family Expression in Patients with Locally Advanced Rectal Cancer Following Neoadjuvant Chemoradiotherapy.OncoTargets and therapy · 2020Article
- Paclitaxel's Mechanistic and Clinical Effects on Breast Cancer.Biomolecules · 2019Review
- Review
- Forkhead box K2 promotes human colorectal cancer metastasis by upregulating ZEB1 and EGFR.Theranostics · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The forkhead transcription factor FOXK2 plays a critical role in suppressing tumorigenesis and mediating cytotoxic drug action in breast cancer. However, the mechanism by which the biological function of FOXK2 is regulated remains poorly understood. Here, we investigated the role of SUMOylation in modulating FOXK2-mediated drug sensitivity. We identified SUMOylation consensus motifs within the FOXK2 sequence and constructed two SUMOylation-defective double mutants by converting lysine 527 and 633 to arginines and glutamic acid 529 and 635 to alanines, respectively. We found that both the FOXK2 SUMOylation-deficient (K527/633 R) and (E529/635 A) mutants were ineffective in mediating the cytotoxic function of paclitaxel when compared to the wild-type (WT) FOXK2. When overexpressed, unlike the wild-type (WT) FOXK2, the K527/633 R mutant had little effect on the sensitivity of MCF-7 and MDA-MB-231 cells to paclitaxel, as examined by cell viability and clonogenic assays. Our results also showed that MCF-7 cells overexpressing the K527/633 R mutant form of FOXK2 or the empty expression vector have lower protein and mRNA levels of its tumour suppressive transcriptional target FOXO3 compared to the wild-type FOXK2. Consistently, ChIP assays revealed that unlike wild-type FOXK2, the SUMOylation-defective (K527/633 R) mutant is unable to bind to the FOXO3 promoter, despite expressing comparable levels of protein and having the same subcellular localization as the wild-type FOXK2 in MCF-7 cells. Interestingly, expression of neither the wild-type nor the K527/633 R mutant FOXK2 had any effect on the proliferation and paclitaxel sensitivity of the MCF-7 Tax
Identifiers
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.