Knockdown of zinc finger protein, X-linked (ZFX) inhibits cell proliferation and induces apoptosis in human laryngeal squamous cell carcinoma

2011 ◽  
Vol 360 (1-2) ◽  
pp. 301-307 ◽  
Author(s):  
Jugao Fang ◽  
Zhenkun Yu ◽  
Meng Lian ◽  
Hongzhi Ma ◽  
Jun Tai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Zinc Finger ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Protein X

scholarly journals Hypermethylation of a Cluster of Krüppel-Type Zinc Finger Protein Genes on Chromosome 19q13 in Oropharyngeal Squamous Cell Carcinoma

2011 ◽  
Vol 178 (5) ◽  
pp. 1965-1974 ◽  
Author(s):  
Roberto A. Lleras ◽  
Leslie R. Adrien ◽  
Richard V. Smith ◽  
Benjamin Brown ◽  
Naheed Jivraj ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Zinc Finger ◽  
Squamous Cell ◽  
Zinc Finger Protein ◽  
Oropharyngeal Squamous Cell Carcinoma ◽  
Finger Protein ◽  
Chromosome 19Q13

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 ZNF282 (Zinc finger protein 282), a novel E2F1 co-activator, promotes esophageal squamous cell carcinoma

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 ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Zinc Finger ◽  
Squamous Cell ◽  
Zinc Finger Protein ◽  
Finger Protein

scholarly journals Dysregulation of zinc finger protein, X-linked (ZFX) impairs cell proliferation and induces apoptosis in human oral squamous cell carcinorma

Tumor Biology ◽  
2015 ◽  
Vol 36 (8) ◽  
pp. 6103-6112 ◽  
Author(s):  
Hongzhi Ma ◽  
Fan Yang ◽  
Meng Lian ◽  
Ru Wang ◽  
Haizhou Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Zinc Finger ◽  
Squamous Cell ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Protein X

Tra2β silencing suppresses cell proliferation in laryngeal squamous cell carcinoma via inhibiting PI3K/AKT signaling

2018 ◽  
Vol 129 (9) ◽  
Author(s):  
Hao‐Sheng Ni ◽  
Song‐Qun Hu ◽  
Xi Chen ◽  
Yi‐Fei Liu ◽  
Ting‐Ting Ni ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Akt Signaling

scholarly journals Targeting SKA3 suppresses the proliferation and chemoresistance of laryngeal squamous cell carcinoma via impairing PLK1–AKT axis-mediated glycolysis

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Wei Gao ◽  
Yuliang Zhang ◽  
Hongjie Luo ◽  
Min Niu ◽  
Xiwang Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Critical Role ◽  
In Vivo Experiments ◽  
Potential Strategy

Abstract Spindle and kinetochore-associated complex subunit 3 (SKA3) is a well-known regulator of chromosome separation and cell division, which plays an important role in cell proliferation. However, the mechanism of SKA3 regulating tumor proliferation via reprogramming metabolism is unknown. Here, SKA3 is identified as an oncogene in laryngeal squamous cell carcinoma (LSCC), and high levels of SKA3 are closely associated with malignant progression and poor prognosis. In vitro and in vivo experiments demonstrate that SKA3 promotes LSCC cell proliferation and chemoresistance through a novel role of reprogramming glycolytic metabolism. Further studies reveal the downstream mechanisms of SKA3, which can bind and stabilize polo-like kinase 1 (PLK1) protein via suppressing ubiquitin-mediated degradation. The accumulation of PLK1 activates AKT and thus upregulates glycolytic enzymes HK2, PFKFB3, and PDK1, resulting in enhancement of glycolysis. Furthermore, our data reveal that phosphorylation at Thr360 of SKA3 is critical for its binding to PLK1 and the increase in glycolysis. Collectively, the novel oncogenic signal axis “SKA3-PLK1-AKT” plays a critical role in the glycolysis of LSCC. SKA3 may serve as a prognostic biomarker and therapeutic target, providing a potential strategy for proliferation inhibition and chemosensitization in tumors, especially for LSCC patients with PLK1 inhibitor resistance.

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