scholarly journals In-vivo imaging of oral squamous cell carcinoma by EGFR monoclonal antibody conjugated near-infrared quantum dots in mice

2011 ◽  
pp. 1739 ◽  
Author(s):  
Kai Yang
Keyword(s):  
Monoclonal Antibody ◽  
Quantum Dots ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
In Vivo Imaging ◽  
Near Infrared

Quantum dot-based visual in vivo imaging for oral squamous cell carcinoma in mice

Oral Oncology ◽  
2010 ◽  
Vol 46 (12) ◽  
pp. 864-868 ◽  
Author(s):  
Kai Yang ◽  
Yu-An Cao ◽  
Chunmeng Shi ◽  
Zhi-Gang Li ◽  
Fu-Jun Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Quantum Dot ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
In Vivo Imaging

scholarly journals Effects of lentivirus-mediated shRNA targeting integrin-linked kinase on oral squamous cell carcinoma in vitro and in vivo

2015 ◽  
Vol 35 (1) ◽  
pp. 89-98 ◽  
Author(s):  
LIN QUE ◽  
DAN ZHAO ◽  
XIU-FA TANG ◽  
JI-YUAN LIU ◽  
XIANG-YU ZHANG ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Integrin Linked Kinase

scholarly journals Synergetic Effects of PARP Inhibitor AZD2281 and Cisplatin in Oral Squamous Cell Carcinoma in Vitro and in Vivo

2016 ◽  
Vol 17 (3) ◽  
pp. 272 ◽  
Author(s):  
Masaaki Yasukawa ◽  
Hisako Fujihara ◽  
Hiroaki Fujimori ◽  
Koji Kawaguchi ◽  
Hiroyuki Yamada ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Parp Inhibitor ◽  
Synergetic Effects

Shrinkage in oral squamous cell carcinoma: An analysis of tumor and margin measurements in vivo , post-resection, and post-formalin fixation

2017 ◽  
Vol 38 (6) ◽  
pp. 660-662 ◽  
Author(s):  
Lauren A. Umstattd ◽  
Jonathan C. Mills ◽  
William A. Critchlow ◽  
Gregory J. Renner ◽  
Robert P. Zitsch
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Formalin Fixation

scholarly journals Knockdown of circ_0011946 targets miR-216a-5p/BCL2L2 axis to regulate proliferation, migration, invasion and apoptosis of oral squamous cell carcinoma cells

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Zhou ◽  
Shuhong Zhang ◽  
Zhonghan Min ◽  
Zhongwei Yu ◽  
Huaiwei Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
B Cell Lymphoma ◽  
Luciferase Reporter ◽  
Migration And Invasion

Abstract Background Circular RNAs (circRNAs) are implicated in the development of oral squamous cell carcinoma (OSCC). The aim of current research is to elucidate the role and mechanism of circ_0011946 in the functional behaviors of OSCC cells. Methods Circ_0011946, microRNA (miR)-216a-5p, B cell lymphoma-2-like 2 protein (BCL2L2) abundances were exposed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation, migration, invasion and apoptosis were detected by MTT, colony formation assay, transwell, wound-healing and flow cytometry assays, respectively. Target correlation was tested by dual-luciferase reporter and RNA pull-down assays. An in vivo xenograft experiment was employed to investigate the function of circ_0011946 on tumor growth in vivo. Results Circ_0011946 and BCL2L2 levels were increased, while miR-216a-5p level was decreased in OSCC tissues and cells. Circ_0011946 knockdown impeded proliferation, migration, and invasion, but promoted apoptosis in OSCC cells. Circ_0011946 functioned as a sponge for miR-216a-5p, and BCL2L2 was targeted by miR-216a-5p. Besides, miR-216a-5p or BCL2L2 knockdown partly attenuated the inhibitory influences of circ_0011946 silence or miR-216a-5p overexpression on OSCC cell progression. Furthermore, circ_0011946 post-transcriptionally regulated BCL2L2 through sponging miR-216a-5p. Moreover, circ_0011946 knockdown constrained OSCC tumor growth in vivo. Conclusion Circ_0011946 silence repressed OSCC cell proliferation, migration, and invasion, but promoted apoptosis through the regulation of the miR-216a-5p/BCL2L2 axis.

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