scholarly journals Retraction of: Elevated Expression of Zinc Finger Protein 703 Promotes Cell Proliferation and Metastasis through PI3K/AKT/GSK-3β Signalling in Oral Squamous Cell Carcinoma

2021 ◽  
Vol 55 (1) ◽  
pp. 138-138
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Elevated Expression ◽  
Proliferation And Metastasis ◽  
Gsk 3Β ◽  
Cell Proliferation And Metastasis

Salivary zinc finger protein 510 peptide as a novel biomarker for detection of oral squamous cell carcinoma in early stages

2011 ◽  
Vol 412 (15-16) ◽  
pp. 1357-1365 ◽  
Author(s):  
Yu-Jen Jou ◽  
Chia-Der Lin ◽  
Chih-Ho Lai ◽  
Chih-Hsin Tang ◽  
Su-Hua Huang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Zinc Finger ◽  
Squamous Cell ◽  
Zinc Finger Protein ◽  
Early Stages ◽  
Finger Protein

Resveratrol suppresses malignant progression of oral squamous cell carcinoma cells by inducing the ZNF750 pathway

2021 ◽  
Author(s):  
Yanjun Duan ◽  
Yongjie Wang ◽  
Xiaojia Yin ◽  
Yue Xiao
Keyword(s):  
Squamous Cell Carcinoma ◽  
Growth Factor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Zinc Finger ◽  
Squamous Cell ◽  
Colony Formation ◽  
Zinc Finger Protein ◽  
Carcinoma Cells ◽  
Finger Protein

Abstract Deletion or mutation of zinc finger protein 750 (ZNF750) has been linked to oral squamous cell carcinoma (OSCC), but it is not clear whether ZNF750 is a therapeutic target for OSCC. This study examined whether activation of zinc finger protein 750 (ZNF750) pathway may be involved in the ability of resveratrol to inhibit malignant progression of CAL-27 oral squamous cell carcinoma cells. CAL-27 cells were treated with resveratrol and transfected with plasmids expressing a ZNF750 mimic or ZNF750 inhibitor. Cell proliferation was assessed using the CCK-8 assay and a BrdU ELISA, and cell cycle distribution and apoptosis were examined using flow cytometry. Colony formation was also assessed. Western blotting was used to examine the effects of resveratrol on levels of angiogenin, vascular endothelial growth factor (VEGF), prolyl hydroxylase 2 (PHD2), G protein signal-regulated protein 5 (RGS5), integrin A5 (ITGA5), integrin B1 (ITGB1), CD44 and ZNF750. Quantitative PCR was used to examine effects on mRNA levels of platelet derived growth factor (PDGFB) and tumor vascular marker CD105. Resveratrol down-regulated angiogenin, VEGF, RGS5, CD105, and the cell adhesion molecules ITGA5, ITGB1 and CD44 in CAL-27 cells. Conversely, it up-regulated ZNF750, PHD2 and PDGFB. These changes were associated with reduced proliferation, reduced colony formation and increased apoptosis. ZNF750 silencing partly reversed these effects of resveratrol. The ability of resveratrol to suppress progression of oral squamous cell carcinoma may involve activation of the ZNF750 pathway and modification of the tumor vascular microenvironment.

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.

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.

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

2020 ◽  
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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