scholarly journals miR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism

2014 ◽  
Vol 33 (2) ◽  
pp. 974-980 ◽  
Author(s):  
JING CAO ◽  
TAO GUO ◽  
QINGSHAN DONG ◽  
JIANQIANG ZHANG ◽  
YANFENG LI
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tongue Squamous Cell Carcinoma ◽  
Human Tongue ◽  
Proliferation And Metastasis ◽  
Cox 2 ◽  
Cell Proliferation And Metastasis ◽  
Dependent Mechanism

scholarly journals Linc01234 promotes cell proliferation and metastasis in oral squamous cell carcinoma via miR-433/PAK4 axis

2019 ◽  
Author(s):  
Deyu LIU ◽  
xinchun jian ◽  
PU XU ◽  
Rong ZHU ◽  
Yuan WANG
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Clinical Importance ◽  
Migration And Invasion ◽  
Lymphnode Metastasis ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

Abstract Background Mounting studies demonstrate long non-coding RNAs (lncRNAs) play an important role in tumor progression. However, the potential biological functions and clinical importance of linc01234 in oral squamous cell carcinoma (OSCC) still remain unclear. Methods Two OSCC cells were transfected with siRNAs targeting linc01234, and RT-qPCR, CCK-8, EDU, wound healing and Transwell and western blot assays were performed to analyze the effect of linc01234 on cell proliferation, migration and invasion. Bioinformatic analysis, luciferase assays and RT-qPCR identified a competitive endogenous RNAs (ceRNAs) among linc01234, miR-433-3p and PAK4. Results We found that linc01234 was significantly upregulated in OSCC tissues and cell lines and positively associated with T stage, lymphnode metastasis, differentiation. Kaplan-Meier analysis of OSCC reveals a positive correlation between linc01234 and the overall survival. Following the linc01234 deletion, the cell proliferation and metastasis abilities in CAL27 and SCC25 cells were found to be extremely reduced. Mechanism studies indicated that linc01234 located in cytoplasm and shared microRNA (miRNA) response elements with miR-433-3p. Luciferase assays indicated that miR-433-3p bind to the 3′-UTR of PAK4. Conclusions Our results indicated that linc01234 functioned as an oncogene in OSCC and might be a potential therapeutic target for OSCC.

scholarly journals Linc01234 promotes cell proliferation and metastasis in oral squamous cell carcinoma via miR-433/PAK4 axis

2019 ◽  
Author(s):  
Deyu LIU ◽  
xinchun jian ◽  
PU XU ◽  
Rong ZHU ◽  
Yuan WANG
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Luciferase Reporter ◽  
Lymphnode Metastasis ◽  
Repressive Effect ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

Abstract Background: Mounting studies demonstrate long non-coding RNA s ( lncRNAs ) play an important role in tumor progression. However, the potential biological functions and clinical importance of Linc01234 in oral squamous cell carcinoma ( OSCC ) still remain unclear. Methods: We evaluated the expression profile and prognostic values of Linc01234 in OSCC tissues via RT-qPCR. Then, functional experiments in vitro were performed to investigate the effects of Linc01234 on tumor growth, migration and invasion in OSCC. Mechanistically, RT-qPCR, bioinformatic analysis and dual luciferase reporter assays were performed to identify a competitive endogenous RNA s ( ceRNA s) among Linc01234, miR-433-3p and PAK4. Results: We found that Linc01234 was evidently upregulated in OSCC tissues and cell lines, and its level was positively associated with T stage, lymphnode metastasis, differentiation and poor prognosis of patients with OSCC. Our results found that Linc01234 inhibited cell proliferation and metastasis abilities in CAL27 and SCC25 cells following its deletion. Mechanistic analysis indicated that Linc01234 may act as a ceRNA (competing endogenous RNA) of miR-433-3p to relieve the repressive effect of miR-433-3p on its target PAK4. Conclusions: Our results indicated that Linc01234 promotes OSCC progression through Linc01234/miR-433/PAK4 axis and might be a potential therapeutic target for OSCC.

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