scholarly journals CDKN1A‑interacting zinc finger protein 1 is a novel biomarker for lung squamous cell carcinoma

2017 ◽  
Author(s):  
Xiaojun Zhou ◽  
Qiang Liu ◽  
Youichiro Wada ◽  
Lin Liao ◽  
Ju Liu
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 ◽  
...  

2021 ◽  
Author(s):  
Yanjun Duan ◽  
Yongjie Wang ◽  
Xiaojia Yin ◽  
Yue Xiao

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.


Oncotarget ◽  
2014 ◽  
Vol 5 (23) ◽  
pp. 12260-12272 ◽  
Author(s):  
So-Young Yeo ◽  
Sang Yun Ha ◽  
Eun Ji Yu ◽  
Keun-Woo Lee ◽  
Jeong Hoon Kim ◽  
...  

Author(s):  
Zheng Dong ◽  
Qing-Hua Xu ◽  
Yuan-Bin Zhu ◽  
Yong-Feng Wang ◽  
Jie Xiong ◽  
...  

Aims : The present study explored the clinical significance of microRNA-22 (miR-22) expression in lung squamous cell carcinoma and to explore the targeting relationship with vascular endothelial growth factor receptor 3 (VEGFR3). Methods: A total of 49 patients with lung squamous cell carcinoma who underwent surgical treatment was selected. The expression of miR-22 was detected by fluorescence quantitative real-time PCR (qPCR), the expression of VEGFR3 was detected by Western blotting assays, and D240 labeled microlymphatic vessels density (MLVD) was detected immunohistochemistry (IHC). Lung squamous cell carcinoma cell line SK-MES-1 was selected and the targeting relationship between miR-22 and VEGFR3 was analyzed by double luciferase reporter gene assay. Western blotting assays were used to detect the expression of vascular endothelial growth factor-D (VEGF-D) and D240 in the blank control group, empty vector transfection group, miR-22 transfection group, miR-22 and VEGFR3 co-transfection group. Results: The expression range of miR-22 in lung squamous cell carcinoma was 0.8-3.5. The expression of miR-22 in lung squamous cell carcinoma was significantly different by tumor maximum diameter, lymph node metastasis, vascular invasion and TNM stage. The expression of miR-22 was linked to survival time. There was a negative correlation between miR-22 and VEGFR3, miR-22 and MLVD. Double luciferase reporter gene assays showed that miR-22 reduced the luciferase activity of pGL3-VEGFR3-WT transfected cells. Compared with the control group, the expression of VEGF-D and D2-40 in the miR-22 transfection group was significantly decreased. However, VEGF-D and D240 in the miR-22 and VEGFR3 cotransfection group reversed the changes. Conclusion: We assumed that the abnormal expression of miR-22 in lung squamous cell carcinoma may be involved in the development and progression of lung squamous cell carcinoma. MiR-22 negatively regulated the target gene VEGFR3 to mediate lymphangiogenesis. The expression of miR-22 may also be linked to the prognosis of the disease.


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