miR‐19a may function as a biomarker of oral squamous cell carcinoma (OSCC) by regulating the signaling pathway of miR‐19a/GRK6/GPCRs/PKC in a Chinese population

BackgroundIn this study, we aimed to investigate the potential of miR‐19a as a biomarker of OSCC and its underlying molecular mechanisms.MethodsWe collected serum and saliva samples from 66 OSCC patients and 66 healthy control subjects. Real‐time PCR analysis, bioinformatic analysis and luciferase a...

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Veröffentlicht in:Journal of oral pathology & medicine 2023-11, Vol.52 (10), p.971-979
Hauptverfasser: Chen, Jijun, Wang, Liang, Ma, Danhua, Zhang, He, Fan, Jiayan, Gao, Hongyan, Xia, Xinyu, Wu, Wei, Shi, Yuyuan
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Sprache:eng
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Zusammenfassung:BackgroundIn this study, we aimed to investigate the potential of miR‐19a as a biomarker of OSCC and its underlying molecular mechanisms.MethodsWe collected serum and saliva samples from 66 OSCC patients and 66 healthy control subjects. Real‐time PCR analysis, bioinformatic analysis and luciferase assays were performed to establish a potential signaling pathway of miR‐19a/GRK6/GPCRs/PKC. Flowcytometry and Transwell assays were performed to observe the changes in cell apoptosis, metastasis and invasion.ResultsWe found that miR‐19a, GPR39 mRNA and PKC mRNA were upregulated while GRK6 mRNA was downregulated in the serum and saliva samples collected from OSCC patients. Moreover, in silico analysis confirmed a potential binding site of miR‐19a on the 3′UTR of GRK6 mRNA, and the subsequent luciferase assays confirmed the molecular binding between GRK6 and miR‐19a. We further identified that the over‐expression of miR‐19a could regulate the signaling between GRK6, GPR39 and PKC via the signaling pathway of miR‐19a/GRK6/GPR39/PKC, which accordingly resulted in suppressed cell apoptosis and promoted cell migration and invasion.ConclusionCollectively, the findings of our study propose that miR‐19a is a crucial mediator in the advancement of OSCC, offering a potential avenue for the development of innovative therapeutic interventions aimed at regulating GRK6 and its downstream signaling pathways.
ISSN:0904-2512
1600-0714
DOI:10.1111/jop.13478