scholarly journals Potential molecular mechanism of radiation-induced cytotoxicity of Cetrimonium bromide to head and neck cancer cells

2021 ◽  
Vol 16 (3) ◽  
pp. 241-244
Author(s):  
Jian Zhang

A previous study has shown that Cetrimonium bromide has a slight cytotoxicity to head and neck cancer cells due to the presence of the cationic quaternary amine group in this molecule that affects the function of mitochondria.The same study also found that the cytotoxicity of Cetrimonium bromide increased when combined with gamma radiation and this could be used to treat head and neck cancer in a mice in vivo tumor model.In the current study, an in vitro photochemical reaction between Cetrimonium chloride and tyrosine was investigated in order to understand the molecular mechanism of the in vivo observations and data. I found that Cetrimonium chloride could react with tyrosine upon simulated solar irradiation to produce an imine Schiff base which turned into cyano-tyrosine and a melanin polymer.It is possible that in the in vivo study mentioned earlier, the gamma radiation and Cetrimonium bromide together destroyed the tyrosine residues in some cellular proteins chemically, and as a result, tyrosine phosphorylation was inhibited in the cancer cells which slowed the growth of the tumor.

Biomolecules ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 599
Author(s):  
Song-Hee Kim ◽  
Byung-Chul Kang ◽  
Daseul Seong ◽  
Won-Hyeok Lee ◽  
Jae-Hee An ◽  
...  

EPHA3, a member of the EPH family, is overexpressed in various cancers. We demonstrated previously that EPHA3 is associated with radiation resistance in head and neck cancer via the PTEN/Akt/EMT pathway; the inhibition of EPHA3 significantly enhances the efficacy of radiotherapy in vitro and in vivo. In this study, we investigated the mechanisms of PTEN regulation through EPHA3-related signaling. Increased DNA methyltransferase 1 (DNMT1) and enhancer of zeste homolog 2 (EZH2) levels, along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, correlated with decreased levels of PTEN in radioresistant head and neck cancer cells. Furthermore, PTEN is regulated in two ways: DNMT1-mediated DNA methylation, and EZH2-mediated histone methylation through EPHA3/C-myc signaling. Our results suggest that EPHA3 could display a novel regulatory mechanism for the epigenetic regulation of PTEN in radioresistant head and neck cancer cells.


2019 ◽  
Vol 60 (3) ◽  
pp. 289-297 ◽  
Author(s):  
Agata Abramowicz ◽  
Anna Wojakowska ◽  
Lukasz Marczak ◽  
Malgorzata Lysek-Gladysinska ◽  
Mateusz Smolarz ◽  
...  

2020 ◽  
Vol 19 (9) ◽  
pp. 1955-1955
Author(s):  
Abu Syed Md Anisuzzaman ◽  
Abedul Haque ◽  
Dongsheng Wang ◽  
Mohammad Aminur Rahman ◽  
Chao Zhang ◽  
...  

2012 ◽  
Vol 103 ◽  
pp. S371
Author(s):  
J. Bussink ◽  
J.H.A.M. Kaanders ◽  
D.L. Wheeler ◽  
A.J. van der Kogel ◽  
M. Iida ◽  
...  

2014 ◽  
Vol 90 (8) ◽  
pp. 678-686 ◽  
Author(s):  
Iris Eke ◽  
Mirjam Ingargiola ◽  
Claudia Förster ◽  
Leoni A. Kunz-Schughart ◽  
Michael Baumann ◽  
...  

Oral Oncology ◽  
2007 ◽  
Vol 43 (4) ◽  
pp. 358-365 ◽  
Author(s):  
Ting-Hua Yang ◽  
Chin-Tin Chen ◽  
Cheng-Ping Wang ◽  
Pei-Jen Lou

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 6078-6078
Author(s):  
R. Rodríguez-Barrueco ◽  
M. Ortíz-Ruiz ◽  
J. J. Cruz ◽  
A. Ocana ◽  
A. Pandiella

6078 Background: Squamous cell carcinoma of the head and neck (SCCHN) is still an incurable disease in the metastatic setting. A particular subgroup of proteins implicated in the head and neck cancer are the tyrosine kinases (TK). Therapeutic inhibition of several of them including the EGF receptor with cetuximab in combination with radiotherapy or chemotherapy has shown to be clinically useful. Beyond EGFR, oncogenic activation of other TKs may be implicated in the genesis/progression of SCCHN. In this context, the identification of the TKs activated in SCCHN is a must in order to adequately target these kinases with already available inhibitors. Methods: Here we have investigated activated tyrosine kinases in head and neck cancer tumors derived from patients using a human phospho protein array for 42 receptor tyrosine kinases (RTK). Western-blot experiments were performed to validate each phospho RTK in tumors from patients. The same approach was followed in a series of head and neck cancer cell lines. In vivo xenografted models were used to study the antiproliferative effect of the combination of specific TK inhibitors against them. Results: TK receptors of the EGF and the VEGF family were the mostly activated in tumors derived from patients. 90% of patients revealed high pEGFR content. In addition, other EGFR/HER family receptors, such as HER3, were also activated (phosphorylated) in samples from patients. These data were corroborated in the SCCHN cell lines. In these cells, other RTK signalling intermediates were also active. Particularly, the Akt and FAK kinases. Combination of the anti-EGFR-HER2 TK inhibitor lapatinib with dasatinib (that targets FAK) was synergistic in vitro. Combination of lapatinib with the anti-VEGFR TK inhibitor pazopanib was inefficient in vitro, but resulted in a better trend in response in the in vivo xenografted models, as compared to the action of the single agents. Conclusions: Rational target drug combinations should be based on the identification of activated TK receptors or downstream signalling molecules. In head and neck cancer combination strategies using anti-EGFR/HER, anti-FAK, and anti-VEGFR compounds increases the action of individual treatments. These results open the door for future clinical development of these drug combinations. No significant financial relationships to disclose.


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