ArticleJournal of cancer research and clinical oncology2017
GLI-mediated Keratin 17 expression promotes tumor cell growth through the anti-apoptotic function in oral squamous cell carcinomas.
Article in Journal of cancer research and clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Association ofJournal of dental sciences · 2026Article
- Unraveling the Keratin Expression in Oral Leukoplakia: A Scoping Review.International journal of molecular sciences · 2024Article
- A map of signaling responses in the human airway epithelium.Cell systems · 2024Article
- A Kaleidoscope of Keratin Gene Expression and the Mosaic of Its Regulatory Mechanisms.International journal of molecular sciences · 2023Review
- The Role of Zinc Finger Proteins in Various Oral Conditions.TheScientificWorldJournal · 2022Review
- The Role of Keratin17 in Human Tumours.Frontiers in cell and developmental biology · 2022Review
- A pan-cancer analysis of the oncogenic role of Keratin 17 (Translational cancer research · 2021Article
- Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021Review
- SARS-CoV-2-triggered neutrophil extracellular traps mediate COVID-19 pathology.The Journal of experimental medicine · 2020Article
- Merkel Cell Polyomavirus T Antigens Induce Merkel Cell-Like Differentiation in GLI1-Expressing Epithelial Cells.Cancers · 2020Article
- Silencing of keratin 17 by lentivirus-mediated short hairpin RNA inhibits the proliferation of PANC-1 human pancreatic cancer cells.Oncology letters · 2020Article
- The TRPV4-AKT axis promotes oral squamous cell carcinoma cell proliferation via CaMKII activation.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Keratin 17 Suppresses Cell Proliferation and Epithelial-Mesenchymal Transition in Pancreatic Cancer.Frontiers in medicine · 2020Article
- Wnt/β-catenin signaling, which is activated in odontomas, reduces Sema3A expression to regulate odontogenic epithelial cell proliferation and tooth germ development.Scientific reports · 2019Article
- POM121 is identified as a novel prognostic marker of oral squamous cell carcinoma.Journal of Cancer · 2019Article
- Overexpression of KRT17 promotes proliferation and invasion of non-small cell lung cancer and indicates poor prognosis.Cancer management and research · 2019Article
- Retinoids induce antagonism between FOXO3A and FOXM1 transcription factors in human oral squamous cell carcinoma (OSCC) cells.PloS one · 2019Article
- GLI3 knockdown decreases stemness, cell proliferation and invasion in oral squamous cell carcinoma.International journal of oncology · 2018Article
- Keratin 17 Promotes Lung Adenocarcinoma Progression by Enhancing Cell Proliferation and Invasion.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeKeratin 17 (KRT17) has been suggested as a potential diagnostic marker of squamous cell carcinoma including oral squamous cell carcinoma (OSCC). The current study was conducted to clarify the function of KRT17 and its expression mechanism in OSCC.
methodsImmunohistochemical analyses were carried out to examine the expression of KRT17, GLI family zinc finger (GLI)-1, GLI-2, or cleaved caspase-3 in OSCCs. The expression of KRT17, GLI-1, or GLI-2 was investigated among OSCC cell lines, and the effects of loss-of-function of KRT17 or GLI, using siRNA or inhibitor, on the cell growth of the OSCC cell line HSC-2 particularly with respect to apoptosis were examined.
resultsImmunohistochemical analyses of tissue specimens obtained from 78 OSCC patients revealed that KRT17 was not observed in non-tumor regions but was strongly expressed at high frequencies in tumor regions. Knockdown of KRT17 increased the number of cleaved caspase-3-positive cells, leading to the reduction of cell number. Loss-of-function of GLI-1 or GLI-2 also increased the cell numbers of apoptotic cells positive for staining of Annexin-V and propidium iodide (PI) and the terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling (TUNEL) method, and induced DNA fragmentation. This inhibitory effect on cell growth was partially rescued by exogenous KRT17 expression. In the KRT17-positive regions in OSCCs, GLI-1 or GLI-2 was frequently detected, and the number of cells with cleaved caspase-3 positive was decreased.
conclusionsKRT17 promotes tumor cell growth, at least partially, through its anti-apoptotic effect as a result of the KRT17 overexpression by GLIs in OSCC.
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