scholarly journals Molecular Markers of Anticancer Drug Resistance in Head and Neck Squamous Cell Carcinoma: A Literature Review

Cancers ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 376 ◽  
Author(s):  
Sandra López-Verdín ◽  
Jesús Lavalle-Carrasco ◽  
Ramón Carreón-Burciaga ◽  
Nicolás Serafín-Higuera ◽  
Nelly Molina-Frechero ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Excision Repair ◽  
Dna Lesions ◽  
Neck Squamous Cell Carcinoma ◽  
Tumor Resistance ◽  
Base Excision

This manuscript provides an update to the literature on molecules with roles in tumor resistance therapy in head and neck squamous cell carcinoma (HNSCC). Although significant improvements have been made in the treatment for head and neck squamous cell carcinoma, physicians face yet another challenge—that of preserving oral functions, which involves the use of multidisciplinary therapies, such as multiple chemotherapies (CT) and radiotherapy (RT). Designing personalized therapeutic options requires the study of genes involved in drug resistance. This review provides an overview of the molecules that have been linked to resistance to chemotherapy in HNSCC, including the family of ATP-binding cassette transporters (ABCs), nucleotide excision repair/base excision repair (NER/BER) enzymatic complexes (which act on nonspecific DNA lesions generated by gamma and ultraviolet radiation by cross-linking and forming intra/interchain chemical adducts), cisplatin (a chemotherapeutic agent that causes DNA damage and induces apoptosis, which is a paradox because its effectiveness is based on the integrity of the genes involved in apoptotic signaling pathways), and cetuximab, including a discussion of the genes involved in the cell cycle and the proliferation of possible markers that confer resistance to cetuximab.

scholarly journals XPD c.934G>A polymorphism of nucleotide excision repair pathway in outcome of head and neck squamous cell carcinoma patients treated with cisplatin chemoradiation

Oncotarget ◽  
2016 ◽  
Vol 8 (10) ◽  
pp. 16190-16201 ◽  
Author(s):  
Leisa Lopes-Aguiar ◽  
Ericka Francislaine Dias Costa ◽  
Guilherme Augusto Silva Nogueira ◽  
Tathiane Regine Penna Lima ◽  
Marília Berlofa Visacri ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Nucleotide Excision Repair ◽  
Squamous Cell ◽  
Excision Repair ◽  
Neck Squamous Cell Carcinoma ◽  
Repair Pathway ◽  
Nucleotide Excision ◽  
Nucleotide Excision Repair Pathway

scholarly journals Simultaneously inactivating Src and AKT by saracatinib/capivasertib co-delivery nanoparticles to improve the efficacy of anti-Src therapy in head and neck squamous cell carcinoma

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Liwei Lang ◽  
Chloe Shay ◽  
Xiangdong Zhao ◽  
Yuanping Xiong ◽  
Xuli Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Tumor Targeting ◽  
3D Culture ◽  
Neck Squamous Cell Carcinoma ◽  
Therapeutic Effects ◽  
Tumor Resistance ◽  
Akt Inhibitor

Abstract Background Src, an oncoprotein that drives progression of head and neck squamous cell carcinoma (HNSCC), is commonly hyperactivated in this disease. Unfortunately, the clinical benefit of targeting Src is significantly dampened in HNSCC patients, because the cytotoxic effects of anti-Src therapy and tumor resistance to it are less predictable. Thus, understanding the mechanism of tumor resistance to Src inhibition and seeking a way to overcome it are warranted. Methods Dual drug-loaded nanoparticles (NPs) were developed to co-deliver Src inhibitor saracatinib (AZD0530) and AKT inhibitor capivasertib (AZD5363) into the same population of tumor cells. An orthotopic tongue tumor model was generated to evaluate the in vivo therapeutic effects. Cell growth was determined by CellTiter-Glo® Luminescent Cell Viability Kit, colony formation, and 3D culture, and tumor growth was determined by bioluminescence and tumor size. The molecular changes induced by the treatments were assessed by Western blotting and immunohistochemistry. Results Capivasertib inactivated the AKT-S6 signaling and re-sensitized saracatinib-resistant HNSCC cells to saracatinib. Combination of capivasertib with saracatinib suppressed HNSCC growth more efficiently than either drug alone. Cathepsin B-sensitive NPs for co-delivering saracatinib and capivasertib significantly improved the efficacy of tumor repression without increasing side effects, which were due to highly specific tumor-targeting drug delivery system and synergistic anticancer effects by co-inactivation of AKT and Src in HNSCC cells. Conclusions Addition of AKT blockade improves anti-HNSCC efficacy of anti-Src therapy, and co-delivery of capivasertib and saracatinib by tumor-targeting NPs has the potential to achieve better treatment outcomes than the free drug combination.

scholarly journals HIF-1α or HOTTIP/CTCF Promotes Head and Neck Squamous Cell Carcinoma Progression and Drug Resistance by Targeting HOXA9

2020 ◽  
Vol 20 ◽  
pp. 164-175 ◽  
Author(s):  
Qiang Sun ◽  
Shuai-Yuan Zhang ◽  
Jun-Fang Zhao ◽  
Xin-Guang Han ◽  
Hai-Bin Wang ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Neck Squamous Cell Carcinoma

scholarly journals The roles of extracellular vesicles in the development, microenvironment, anticancer drug resistance, and therapy of head and neck squamous cell carcinoma

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Xueying Wang ◽  
Junnan Guo ◽  
Pingyang Yu ◽  
Lunhua Guo ◽  
Xionghui Mao ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Immune Escape ◽  
Neck Squamous Cell Carcinoma ◽  
Bioactive Molecules ◽  
Malignant Tumours ◽  
Biological Behaviour

AbstractHead and neck squamous cell carcinoma (HNSCC) is one of the main malignant tumours affecting human health, mainly due to delayed diagnosis and high invasiveness. Extracellular vehicles (EVs) are membranous vesicles released by cells into the extracellular matrix that carry important signalling molecules and stably and widely exist in various body fluids, such as plasma, saliva, cerebrospinal fluid, breast milk, urine, semen, lymphatic fluid, synovial fluid, amniotic fluid, and sputum. EVs transport almost all types of bioactive molecules (DNA, mRNAs, microRNAs (miRNAs), proteins, metabolites, and even pharmacological compounds). These “cargoes” can act on recipient cells, reshaping the surrounding microenvironment and altering distant targets, ultimately affecting their biological behaviour. The extensive exploration of EVs has deepened our comprehensive understanding of HNSCC biology. In this review, we not only summarized the effect of HNSCC-derived EVs on the tumour microenvironment but also described the role of microenvironment-derived EVs in HNSCC and discussed how the “mutual dialogue” between the tumour and microenvironment mediates the growth, metastasis, angiogenesis, immune escape, and drug resistance of tumours. Finally, the clinical application of EVS in HNSCC was assessed.

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