ArticleOncogene2014
Transformation of human ovarian surface epithelial cells by Krüppel-like factor 8.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Mapping and visualization of global research progress on deubiquitinases in ovarian cancer: a bibliometric analysis.Frontiers in pharmacology · 2024Pooled it
- SIRT1 in acute lung injury: unraveling its pleiotropic functions and therapeutic development prospects.Molecular and cellular biochemistry · 2025Review
- Implications of Krüppel-like factor signaling in neuroinflammation for neurodegenerative diseases.American journal of translational research · 2025Review
- The roles of FHL2 in cancer.Clinical and experimental medicine · 2023Review
- Sensitization of breast cancer to Herceptin by redox active nanoparticles.American journal of cancer research · 2021Article
- Role of krüppel-like factor 8 for therapeutic drug-resistant multi-organ metastasis of breast cancer.American journal of cancer research · 2021Article
- Understanding the Complex Milieu of Epithelial-Mesenchymal Transition in Cancer Metastasis: New Insight Into the Roles of Transcription Factors.Frontiers in oncology · 2021Review
- Oncogenes in high grade serous adenocarcinoma of the ovary.Genes & cancer · 2020Article
- KLF7: a new candidate biomarker and therapeutic target for high-grade serous ovarian cancer.Journal of experimental & clinical cancer research : CR · 2020Article
- EMT Factors and Metabolic Pathways in Cancer.Frontiers in oncology · 2020Review
- LncRNA DANCR promotes the proliferation, migration, and invasion of tongue squamous cell carcinoma cells through miR-135a-5p/KLF8 axis.Cancer cell international · 2019Article
- Regulation of Krüppel-like factor 8 by the NEDD4 E3 ubiquitin ligase.American journal of translational research · 2019Article
- Galectin-8 induces partial epithelial-mesenchymal transition with invasive tumorigenic capabilities involving a FAK/EGFR/proteasome pathway in Madin-Darby canine kidney cells.Molecular biology of the cell · 2018Article
- Overexpression of ubiquitin specific proteases 44 promotes the malignancy of glioma by stabilizing tumor-promoter securin.Oncotarget · 2017Article
- Expression of Kruppel-like factor 8 and Ki67 in lung adenocarcinoma and prognosis.Experimental and therapeutic medicine · 2017Article
- Article
- ERK2 phosphorylates Krüppel-like factor 8 protein at serine 48 to maintain its stability.American journal of cancer research · 2016Article
- Antibody-like Biorecognition Sites for Proteins from Surface Imprinting on Nanoparticles.ACS applied materials & interfaces · 2015Article
- KLF8 promotes tumorigenesis, invasion and metastasis of colorectal cancer cells by transcriptional activation of FHL2.Oncotarget · 2015Article
- Identification of epidermal growth factor receptor and its inhibitory microRNA141 as novel targets of Krüppel-like factor 8 in breast cancer.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
We have previously demonstrated that Krüppel-like factor 8 (KLF8) participates in oncogenic transformation of mouse fibroblasts and is highly overexpressed in human ovarian cancer. In this work, we first correlated KLF8 overexpression with the aggressiveness of ovarian patient tumors and then tested if KLF8 could transform human ovarian epithelial cells. Using the immortalized non-tumorigenic human ovarian surface epithelial cell line T80 and retroviral infection, we generated cell lines that constitutively overexpress KLF8 alone or its combination with the known ovarian oncogenes c-Myc, Stat3c and/or Akt and examined the cell lines for anchorage-independent growth and tumorigenesis. The soft agar clonogenic assay showed that T80/KLF8 cells formed significantly more colonies than the mock cells. Interestingly, the cells expressing both KLF8 and c-Myc formed the largest amounts of colonies, greater than the sum of colonies formed by the cells expressing KLF8 and c-Myc alone. These results suggested that KLF8 might be a weak oncogene that works cooperatively with c-Myc to transform ovarian cells. Surprisingly, overexpression of KLF8 alone was sufficient to induce tumorigenesis in nude mice resulting in short lifespan irrespective of whether the T80/KLF8 cells were injected subcutaneously, intraperitoneally or orthotopically into the ovarian bursa. Histopathological studies confirmed that the T80/KLF8 tumors were characteristic of human serous ovarian carcinomas. Comparative expression profiling and functional studies identified the cell cycle regulators cyclin D1 and USP44 as primary KLF8 targets and effectors for the T80 transformation. Overall, we identified KLF8 overexpression as an important factor in human ovarian carcinoma pathogenesis.
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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.