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http://purl.uniprot.org/citations/33378018http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/33378018http://www.w3.org/2000/01/rdf-schema#comment"

Objective

We aimed to clarify the molecular mechanism of how PRKD3 promotes the malignant progression of oral squamous cell carcinoma (OSCC).

Patients and methods

62 cases of OSCC tissues and normal adjacent ones which were further confirmed by a qualified pathologist were collected from patients in the Department of Pathology and Stomatology of our hospital. PRKD3 expression in the above tissue samples was studied by quantitative real-time polymerase chain reaction (qRT-PCR) analysis, and its relationship with clinicopathological characteristics of these OSCC patients was analyzed. Meanwhile, a PRKD3 knockdown expression model was constructed in OSCC cell lines for cell functional experiments. The relationship between PRKD3 and KLF16 was elucidated through bioinformatics and Luciferase reporter gene experiments.

Results

Our data showed that PRKD3 expression in OSCC specimens was remarkably higher than that in adjacent ones. PRKD3 expression showed positive association with the incidence of distant metastasis, but not with other clinical indicators such as gender, age, tumor stage or lymph node metastasis incidence. Patients with high PRKD3 expression had lower overall survival compared to those with low expression. In addition, OSCC cells migration ability and invasiveness were remarkably attenuated after PRKD3 was knocked down. Bioinformatics and Luciferase assay revealed that PRKD3 could directly bind to KLF16 and Western blot suggested that KLF16 was upregulated after PRKD3 was knocked down. In addition, knocking down KLF16 reversed the inhibitory effect of PRKD3 knockdown on invasiveness and metastasis of OSCC cells.

Conclusions

The highly-expressed PRKD3, remarkably associated with metastasis incidence and poor prognosis of OSCC patients, may accelerate the malignant progression of OSCC through modulating KLF16 expression."xsd:string
http://purl.uniprot.org/citations/33378018http://purl.org/dc/terms/identifier"doi:10.26355/eurrev_202012_24169"xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/author"Chen Z."xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/author"Huang Q."xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/author"Xu W."xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/author"Yang J."xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/author"Wang H."xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/author"Zhang L.J."xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/name"Eur Rev Med Pharmacol Sci"xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/pages"12709-12716"xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/title"PRKD3 promotes malignant progression of OSCC by downregulating KLF16 expression."xsd:string
http://purl.uniprot.org/citations/33378018http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/33378018http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/33378018
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