Silencing novel long non-coding RNA FKBP9P1 represses malignant progression and inhibits PI3K/AKT signaling of head and neck squamous cell carcinoma in vitro  

作　　者：Yi-Fan Yang Ling Feng Qian Shi Hong-Zhi Ma Shi-Zhi He Li-Zhen Hou Ru Wang Ju-Gao Fang 

机构地区：[1]Department of Otolaryngology Head and Neck Surgery,Beijing Tongren Hospital,Capital Medical University,Beijing 100730,China [2]Key Laboratory of Otolaryngology Head and Neck Surgery(Ministry of Education of China),Beijing Institute of Otolaryngology,Beijing 100005,China [3]Beijing Key Laboratory of Head and Neck Molecular Diagnostic Pathology,Beijing 100730,China

出　　处：《Chinese Medical Journal》2020年第17期2037-2043,共7页中华医学杂志（英文版）

基　　金：This work was supported by grants from Beijing Municipal Natural Science Foundation(No.7184196);Beijing Municipal Administration of Hospitals’Ascent Plan(No.DFL20180202);Capital Health Development Research Project(No.Shoufa-2018-2-2054);Beijing Natural Science Foundation Program and Scientific Research Key Program of Beijing Municipal Commission of Education(No.KZ201910025034)。

摘　　要：Background:Long non-coding RNAs(lncRNAs)play key roles in human cancers.In our previous study,we demonstrated that lncRNA FKBP prolyl isomerase 9 pseudogene 1(FKBP9P1)was highly expressed in head and neck squamous cell cancer(HNSCC)tissues.However,its functional significance remains poorly understood.In the present study,we identify the role and potential molecular biologic mechanisms of FKBP9P1 in HNSCC.Methods:Quantitative real-time polymerase chain reaction was used to detect the expression of FKBP9P1 in HNSCC tissues,matched adjacent normal tissues,human HNSCC cells(FaDu,Cal-27,SCC4,and SCC9),and human immortalized keratinocytes cell HaCaT(normal control).Cal-27 and SCC9 cells were transfected with sh-FKBP9P1-1,sh-FKBP9P1-2,and normal control(sh-NC)lentivirus.Cell counting kit-8 assay,colony formation assay,wound healing assay,and trans-well assay were used to explore the biologic function of FKBP9P1 in HNSCC cells.Furthermore,western blotting was used to determine the mechanism of FKBP9P1 in HNSCC progression.Chi-squared test was performed to assess the clinical significance among FKBP9P1 high-expression and low-expression groups.Survival analyses were performed using the Kaplan-Meier method and assessed using the log-rank test.The comparison between two groups was analyzed by Student t test,and comparisons among multiple samples were performed by one-way analysis of variance and a Bonferroni post hoc test.Results:FKBP9P1 expression was significantly up-regulated in HNSCC tissues(tumor vs.normal,1.914 vs.0.957,t=7.746,P<0.001)and cell lines(P<0.01 in all HNSCC cell lines).Besides,the median FKBP9P1 expression of HNSCC tissues(1.677)was considered as the threshold.High FKBP9P1 level was correlated with advanced T stage(P=0.022),advanced N stage(P=0.036),advanced clinical stage(P=0.018),and poor prognosis of HNSCC patients(overall survival,P=0.002 and disease-free survival,P<0.001).Knockdown of FKBP9P1 led to marked repression in proliferation,migration,and invasion of HNSCC cells in vitro(P all<0.01).Mechanis

关 键 词：Head and neck squamous cell carcinoma Long non-coding RNA FKBP prolyl isomerase 9 pseudogene 1 PI3K/AKT signaling pathway 

分 类 号：R739.91[医药卫生—肿瘤]