scholarly journals Optical imaging of head and neck squamous cell carcinoma in vivo using arginine-glycine- aspartic acid peptide conjugated near-infrared quantum dots

2013 ◽  
pp. 1779 ◽  
Author(s):  
Kai Yang ◽  
Hao Huang ◽  
Yun-Long Bai ◽  
Hong Tang ◽  
You-Wei Wang
Keyword(s):  
Quantum Dots ◽  
Squamous Cell Carcinoma ◽  
Optical Imaging ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Aspartic Acid ◽  
Squamous Cell ◽  
Near Infrared ◽  
Arginine Glycine Aspartic Acid

scholarly journals In vivo optical imaging of folate receptor-β in head and neck squamous cell carcinoma

2014 ◽  
Vol 124 (8) ◽  
pp. E312-E319 ◽  
Author(s):  
Joel Y. Sun ◽  
Jiayin Shen ◽  
Joel Thibodeaux ◽  
Gang Huang ◽  
Yiguang Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Optical Imaging ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Folate Receptor ◽  
Neck Squamous Cell Carcinoma ◽  
In Vivo Optical Imaging

scholarly journals NIR Imaging of the Integrin-Rich Head and Neck Squamous Cell Carcinoma Using Ternary Copper Indium Selenide/Zinc Sulfide-Based Quantum Dots

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3727
Author(s):  
Ilya Yakavets ◽  
Aurelie Francois ◽  
Maelle Guiot ◽  
Nicolas Lequeux ◽  
Alexandra Fragola ◽  
...  
Keyword(s):  
Quantum Dots ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Near Infrared ◽  
Specific Binding ◽  
Neck Squamous Cell Carcinoma ◽  
Αvβ6 Integrin ◽  
3D Spheroids

The efficient intraoperative identification of cancers requires the development of the bright, minimally-toxic, tumor-specific near-infrared (NIR) probes as contrast agents. Luminescent semiconductor quantum dots (QDs) offer several unique advantages for in vivo cellular imaging by providing bright and photostable fluorescent probes. Here, we present the synthesis of ZnCuInSe/ZnS core/shell QDs emitting in NIR (~750 nm) conjugated to NAVPNLRGDLQVLAQKVART (A20FMDV2) peptide for targeting αvβ6 integrin-rich head and neck squamous cell carcinoma (HNSCC). Integrin αvβ6 is usually not detectable in nonpathological tissues, but is highly upregulated in HNSCC. QD-A20 showed αvβ6 integrin-specific binding in two-dimension (2D) monolayer and three-dimension (3D) spheroid in vitro HNSCC models. QD-A20 exhibit limited penetration (ca. 50 µm) in stroma-rich 3D spheroids. Finally, we demonstrated the potential of these QDs by time-gated fluorescence imaging of stroma-rich 3D spheroids placed onto mm-thick tissue slices to mimic imaging conditions in tissues. Overall, QD-A20 could be considered as highly promising nanoprobes for NIR bioimaging and imaging-guided surgery.

Comparison of in vivo and in vitro prostaglandin E production by squamous cell carcinoma of the head and neck

1994 ◽  
Vol 111 (3) ◽  
pp. 189-196 ◽  
Author(s):  
C SNYDERMAN ◽  
I KLAPAN ◽  
M MILANOVICH ◽  
D HEO ◽  
R WAGNER ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Prostaglandin E

scholarly journals Methyltransferase like 13 mediates the translation of Snail in head and neck squamous cell carcinoma

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Xiaochen Wang ◽  
Kang Li ◽  
Yuehan Wan ◽  
Fangfang Chen ◽  
Maosheng Cheng ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Neck Squamous Cell Carcinoma ◽  
Translation Efficiency ◽  
Mechanism Study ◽  
Clinical Prognosis ◽  
Cellular Phenotypes

AbstractMethyltransferase like 13 (METTL13), a kind of methyltransferase, is implicated in protein binding and synthesis. The upregulation of METTL13 has been reported in a variety of tumors. However, little was known about its potential function in head and neck squamous cell carcinoma (HNSCC) so far. In this study, we found that METTL13 was significantly upregulated in HNSCC at both mRNA and protein level. Increased METTL13 was negatively associated with clinical prognosis. And METTL13 markedly affected HNSCC cellular phenotypes in vivo and vitro. Further mechanism study revealed that METTL13 could regulate EMT signaling pathway by mediating enhancing translation efficiency of Snail, the key transcription factor in EMT, hence regulating the progression of EMT. Furthermore, Snail was verified to mediate METTL13-induced HNSCC cell malignant phenotypes. Altogether, our study had revealed the oncogenic role of METTL13 in HNSCC, and provided a potential therapeutic strategy.

scholarly journals JOSD1 promotes proliferation and chemoresistance of head and neck squamous cell carcinoma under the epigenetic regulation of BRD4

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chao Jing ◽  
Dandan Liu ◽  
Qingchuan Lai ◽  
Linqi Li ◽  
Mengqian Zhou ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Gene Expression Omnibus ◽  
Neck Squamous Cell Carcinoma ◽  
The Cancer Genome Atlas ◽  
In Vivo Experiments

Abstract Background Deubiquitinating enzymes (DUBs) play critical roles in various cancers by modulating functional proteins post-translationally. Previous studies have demonstrated that DUB Josephin Domain Containing 1 (JOSD1) is implicated in tumor progression, however, the role and mechanism of JOSD1 in head and neck squamous cell carcinoma (HNSCC) remain to be explored. In this study, we aimed to identify the clinical significance and function of JOSD1 in HNSCC. Methods The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were analyzed to find novel DUBs in HNSCC. Immunohistochemistry assay was performed to determine the expression of JOSD1 in our cohort of 42 patients suffered with HNSCC. Kaplan–Meier analysis was used to identify the correlation between JOSD1 and the prognosis of HNSCC patients. The regulation of BRD4 on JOSD1 was determined by using pharmacological inhibition and gene depletion. The in vitro and in vivo experiments were conducted to elucidate the role of JOSD1 in HNSCC. Results The results of IHC showed that JOSD1 was aberrantly expressed in HNSCC specimens, especially in the chemoresistant ones. The overexpression of JOSD1 indicated poor clinical outcome of HNSCC patients. Moreover, JOSD1 depletion dramatically impaired cell proliferation and colony formation, and promoted cisplatin-induced apoptosis of HNSCC cells in vitro. Additionally, JOSD1 suppression inhibited the tumor growth and improved chemosensitivity in vivo. The epigenetic regulator BRD4 contributed to the upregulation of JOSD1 in HNSCC. Conclusions These results demonstrate that JOSD1 functions as an oncogene in HNSCC progression, and provide a promising target for clinical diagnosis and therapy of HNSCC.

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