ArticleInternational journal of clinical and experimental pathology2015
Low expression of KLF17 is associated with tumor invasion in esophageal carcinoma.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- KLF family of proteins in gastrointestinal tumors (Review).Oncology letters · 2026Review
- KLF13 promotes esophageal cancer progression and regulates triacylglyceride and free fatty acid metabolism through GPIHBP1.Cell death & disease · 2025Article
- Effect ofThe Journal of international medical research · 2021Article
- CircTADA2A suppresses the progression of colorectal cancer via miR-374a-3p/KLF14 axis.Journal of experimental & clinical cancer research : CR · 2020Article
- Overexpression of KLF17 Predicts a Favorable Prognosis in Patients with Oral Squamous Cell Carcinoma: A Retrospective Study.Medicina (Kaunas, Lithuania) · 2020Article
- Article
- SP and KLF Transcription Factors in Digestive Physiology and Diseases.Gastroenterology · 2017Review
- Up-regulation of KLF17 expression increases the sensitivity of gastric cancer to 5-fluorouracil.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeKLF17 belongs to the Sp/KLF zinc-finger protein family as a regulator in tumor development. However, its expression and biologic function has remained unclear in EC.
methodsThe esophageal carcinoma tissue samples and adjacent normal tissues were obtained from the Second Hospital of Hebei Medical University. Immunohistochemistry, Western blot, and transfection were applied to evaluate the expression and clinical significance of KLF17 in esophageal cancer.
resultsIn this study, we showed that KLF17 was overexpressed in esophageal normal samples compared to the cancer. Moreover, KLF17 was upregulated at lymph node non-metastatic cancer tissues when compared to metastatic cancer tissues. KLF17 overexpression decreased EC cell proliferation, migration and invasion ability. In contrast, the knockdown of KLF17 increased EC cell proliferation, migration and invasion ability.
conclusionThese results suggest that KLF17 inhibits tumor development and may serve as a potential therapeutic target.
Indexed as
Identifiers
26617836PMC4637651W2413107448What OpenQuestion holds
Registered trials
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