ArticleThe Journal of biological chemistry2015
Tumor-suppressive p53 Signaling Empowers Metastatic Inhibitor KLF17-dependent Transcription to Overcome Tumorigenesis in Non-small Cell Lung Cancer.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- KLF18 is a necessary component of the DUX4-initiated transcriptional network and a candidate locus for phenotypic diversity.Genes & development · 2026Article
- Prognostic value of KLFs family genes in renal clear cell carcinoma.Scientific reports · 2024Article
- Abnormal expression of Krüppel-like transcription factors and their potential values in lung cancer.Heliyon · 2024Review
- Kruppel like factor 16 promotes lung adenocarcinoma progression by upregulating lamin B2.Bioengineered · 2022Article
- KLF17 promotes human naïve pluripotency but is not required for its establishment.Development (Cambridge, England) · 2021Article
- Effect ofThe Journal of international medical research · 2021Article
- Krüppel-like factor 17 upregulates uterine corin expression and promotes spiral artery remodeling in pregnancy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Overexpression of KLF17 Predicts a Favorable Prognosis in Patients with Oral Squamous Cell Carcinoma: A Retrospective Study.Medicina (Kaunas, Lithuania) · 2020Article
- High Expression of Long Noncoding RNA PCNA-AS1 Promotes Non-Small-Cell Lung Cancer Cell Proliferation and Oncogenic Activity via Upregulating CCND1.Journal of Cancer · 2020Article
- MIIP inhibits EMT and cell invasion in prostate cancer through miR-181a/b-5p-KLF17 axis.American journal of cancer research · 2020Article
- Krüppel-like factor 17, a novel tumor suppressor: its low expression is involved in cancer metastasis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Low expression of KLF17 is associated with tumor invasion in esophageal carcinoma.International journal of clinical and experimental pathology · 2015Article
- 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
8 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis, which is controlled by concerted action of multiple genes, is a complex process and is an important cause of cancer death. Krüppel-like factor 17 (KLF17) is a negative regulator of metastasis and epithelial-mesenchymal transition (EMT) during cancer progression. However, the underlying molecular mechanism and biological relevance of KLF17 in cancer cells are poorly understood. Here, we show that tumor suppressor protein p53 plays an integral role to induce KLF17 expression in non-small cell lung cancer (NSCLC). p53 is recruited to the KLF17 promoter and results in the formation of p53-DNA complex. p53 enhances binding of p300 and favors histone acetylation on the KLF17 promoter. Mechanistically, p53 physically interacts with KLF17 and thereby enhances the anti-metastatic function of KLF17. p53 empowers KLF17-mediated EMT genes transcription via enhancing physical association of KLF17 with target gene promoters. Nutlin-3 recruits KLF17 to EMT target gene promoters and results in the formation of KLF17-DNA complex via a p53-dependent pathway. p53 depletion abrogates DNA binding affinity of KLF17 to EMT target gene promoters. KLF17 is critical for p53 cellular activities in NSCLC. Importantly, KLF17 enhances p53 transcription to generate a novel positive feedback loop. KLF17 depletion accelerates lung cancer cell growth in response to chemotherapy. Mechanistically, we found that KLF17 increases the expression of tumor suppressor genes p53, p21, and pRB. Functionally, KLF17 required p53 to suppress cancer cell invasion and migration in NSCLC. In conclusion, our study highlights a novel insight into the anti-EMT effect of KLF17 via a p53-dependent pathway in NSCLC, and KLF17 may be a new therapeutic target in NSCLC with p53 status.
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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.