微小RNA200a/141-信号转导和转录激活因子4轴在口腔鳞状细胞癌进展中的作用研究

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[中图分类号]R782 [文献标志码] A [doi] 10.7518/gjkq.2025062

[Abstract]ObjectiveThis study aimed to explore the expresson and clinical significance of mircoRNA （miRNA） 200a/141and signal transducerandactivatorof transcription4 （STAT4） inoralsquamous cellcarcinoma（OSCC）and construct a prognostic model to explore its feasibility asa potential therapeutic target.Invitro experimentsverified that bionic gelatin exosome particles delivered miRNA200a/141toregulateSTAT4.Thisstudyalsoaimed toevaluate the protective capacity and anticancer effects ofnucleicacidsatthecellularandmolecularlevelsof OSCC.MethodsOSCC-related miRNA-sequencing andmessenger RNA-sequencingdatawere downloadedfromThe Cancer Genome Atlas database.Data analysis was performed using R language to assess the expresion levels and clinical correlationof miRNA200a/141 with STAT4.Biomimetic gelatin exosome nanoparticles （GNP-EXO-miRNA200a/141 ）loaded with miRNA were prepared，and Transwellmigrationassy，cellscratchassay，and methyl thiazolyltetrazolium assay were performedto evaluate the effctofnanoparticles on SCC25cels.Theeffectsofthe nanoparticles on STAT4 expression in SCC25 cells were examined usingquantitative polymerase chain reaction and Wester blot. ResultsThe expression of miRNA200a/141 was significantly reduced in OSCC tisses，whereas thatof its target STAT 4 increased，which was inverselycorelated.The preparedGNP-EXO-miRNA20a/141nanoparticles showed good size distributionand stability.Incellexperiments，GNP-EXO-miRNA20a/141significantlyinhibitedtheproliferationandmigrationof SCC25celsand significantlydownregulated STAT4 expresson.ConclusionmiRNA200a/141 plays an importantrole inOSCCbyregulating STAT4，and itis expected tobeapotentialmolecularmarkerand therapeutictarget for the diagnosis， treatment， and prognosis of OSCC.

[Key words]oral squamous cellcarcinoma；mircoRNA200a/141；signal transducer and activatorof transcription 4; exosomes; gelatin nanoparticles

口腔鳞状细胞癌（oralsquamouscellcarcino-ma，OSCC）是一种高侵袭性的肿瘤，占所有口腔恶性肿瘤的 90% 。（剩余15936字）