Overexpressed LncRNA CASC9 Promoted Oral Squamous Cell Carcinoma Cell Proliferation And Migration Via Activating The PI3K/AKT Signaling Pathway

ObjectiveIn recent years,long non-coding RNA(lncRNA)has been found to play an important role in various human cancers.In this study,we explored the expression,function and mechanism of lncRNA CASC9 in oral squamous cell carcinoma(OSCC)in vitro and in vivo.MethodsR language was used to analyze the differential expression of lncRNAs in OSCC and adjacent nocancerous tissues in TCGA database,and the survival curves of dysregulation expressed lncRNAs were analyzed.The expression of CASC9 in OSCC tissues and cell lines was detected by qRT-PCR and in situ hybridization.Chi-square test was used to analyze the correlation between CASC9 expression and clinicopathological features.Kaplan-Meier survival analysis and log-rank test were used to analyze the relationship between the expression of CASC9 and overall survival of patients with OSCC.The expression of PI3 K,AKT and p-AKT weredetected by qRT-PCR and western blot.Cell proliferation,migration,and invasion were detected by CCK8 assay,flow cytometry,and Transwell assay.SCC15 cells with CASC9 knockdown were subcutaneously injected into nude mice to evaluate the effect of CASC9 on tumor growth in vivo.ResultsCASC9 was significantly increased in human OSCC tissues and cell lines(P < 0.05).High expression of CASC9 was remarkably correlated with larger tumor size,advanced clinical stage,high lymphatic metastasis,and poor prognosis of OSCC patients,respectively(P < 0.05).OSCC patients with high expression of CASC9 had poor overall survival(P =0.007).Furthermore,silencing of CASC9 inhibited cell proliferation,migration,and invasion(P < 0.05),and the expression of PI3 K,p-AKT,and MMP-2 was significantly decreased while the expression of P21 was increased(P < 0.05).After adding the PI3 K activator to CASC9 knockdown cells,the proliferation,migration,and expression of the above genes were remarkably rescued(P < 0.05).Downregulation of CASC9 in SCC15 cells significantly suppressed tumorigenesis in vivo.CASC9.ConclusionCASC9 was an independent prognostic factor for OSCC.CASC9 promoted the progression of OSCC by activating the PI3K/AKT signaling pathway.CASC9 may be a novel clinical prognostic marker and therapeutic target for OSCC.