Epigenetic modifications control loss of adhesion and aggressiveness of cancer stem cells derived from head and neck squamous cell carcinoma with intrinsic resistance to cisplatin

Milan, Thaís Moré; Eskenazi, Ana Patrícia Espaladori; Bighetti‐Trevisan, Rayana Longo; Almeida, Luciana O.

doi:10.1016/j.archoralbio.2022.105468

Cited by 8 publications

(5 citation statements)

References 52 publications

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“…CAL27 and SCC9 cells were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA). Cisplatin‐resistant lines (CAL27 CisR , SCC9 CisR ) were established after continuous exposure to cisplatin 29 . The CAL27 cell lineage was cultured in DMEM supplemented with 10% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 mg/mL) (SIGMA, MO, USA) at 37°C in a humidified atmosphere containing 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Cisplatin-resistant lines (CAL27 CisR , SCC9 CisR ) were established after continuous exposure to cisplatin. 29 The CAL27 cell lineage was cultured in DMEM supplemented with 10% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 mg/mL) (SIGMA, MO, USA) at 37 C in a humidified atmosphere containing 5% CO 2 . The SCC9 cell lineage was cultured in DMEM/F-12 supplemented with HEPES solution.…”

Section: Human Oral Cancer Cell Lineages and Culture Conditionsmentioning

confidence: 99%

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FTY720 increases paclitaxel efficacy in cisplatin‐resistant oral squamous cell carcinoma

Torres,

Silva,

Alves

et al. 2023

J Oral Pathology Medicine

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BackgroundOral squamous cell carcinoma has high recurrence and cisplatin resistance. As cancer stem cells, autophagy, and sphingolipids have been appointed as associated with chemotherapy resistance, we tested combined treatments targeting autophagy and/or sphingolipid metabolism with paclitaxel using cisplatin‐resistant oral squamous cell carcinoma cells.MethodsCisplatin‐resistant oral squamous cell carcinoma cells were maintained under exposition to FTY720 and chloroquine combined with paclitaxel and submitted to viability, clonogenicity, and spheres formation assays. The xenograft tumor model using cisplatin‐resistant CAL27 cells was adopted to examine the drug combinations' potential antitumoral efficacy. Using an animal model, sphingolipids profiles from plasma and tissue samples were obtained by liquid chromatography coupled to mass spectrometry to identify potential lipids associated with drug response.Results and DiscussionOur results showed higher autophagic flux in cisplatin‐resistant Ooral squamous cell carcinoma (CAL27 and SCC9) cells than in parental cells. The combinations of an autophagy inhibitor (chloroquine) or an autophagy inducer/sphingosine kinase 1 antagonist (FTY720) with paclitaxel (PTX) had a synergistic antitumor effect. Treated CisR cells lost clonogenicity and tumor sphere abilities and reduced proteins associated with proliferation, survival, and cancer stem cells. FTY720 plus PTX had higher antitumor efficacy than PTX against CAL27 CisR xenograft tumor formation. Additionally, increases in glucosylceramide, dehydroglucosylceramide, and sphingomyelin were presented in responsive tumors.ConclusionFTY720 sensitizes cisplatin‐resistant oral squamous cell carcinoma cells for paclitaxel.

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Section: Methodsmentioning

confidence: 99%

Section: Human Oral Cancer Cell Lineages and Culture Conditionsmentioning

confidence: 99%

FTY720 increases paclitaxel efficacy in cisplatin‐resistant oral squamous cell carcinoma

Torres,

Silva,

Alves

et al. 2023

J Oral Pathology Medicine

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“…Chang et al [41] found positive HDAC2 nuclear staining was detected in 80/93 OSCC samples and 11/20 oral epithelial dysplasia (OED) samples and the labeling index for HDAC2 staining increased substantially from OED (25.8 ± 26.5%) to OSCCs (59.8 ± 28.5%) (p < 0.001) [41]. HDAC2 protein expression was also elevated in advanced, giant tumor size or lymph node metastasis-positive tumors, associated with adhesion loss and invasiveness [42,43]. HDAC2 could maintain HIF-1α stability, promoting oral cancer progression through enhanced cell invasion and migration [44].…”

Section: Classification Hdac Targets and Mechanisms In Hnsccmentioning

confidence: 99%

“…Rastogi et al [68] identified HDAC9 as a target of miR-377 and demonstrated that miR-377 regulates HDAC9 as well as its pro-apoptotic target NR4A1/ Nur77, thereby inhibiting cell growth, inducing apoptosis and reducing migration. The upregulation of HDAC2, HDAC9, SIRT1 and the HDAC1 nuclear distribution contributed to intrinsic resistance, promoting aggressiveness and loss of adhesion of HNSCC [43].…”

Section: Class II Hdacsmentioning

confidence: 99%

Targeting histone deacetylases in head and neck squamous cell carcinoma: molecular mechanisms and therapeutic targets

Xu,

Hou,

et al. 2024

J Transl Med

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The onerous health and economic burden associated with head and neck squamous cell carcinoma (HNSCC) is a global predicament. Despite the advent of novel surgical techniques and therapeutic protocols, there is an incessant need for efficacious diagnostic and therapeutic targets to monitor the invasion, metastasis and recurrence of HNSCC due to its substantial morbidity and mortality. The differential expression patterns of histone deacetylases (HDACs), a group of enzymes responsible for modifying histones and regulating gene expression, have been demonstrated in neoplastic tissues. However, there is limited knowledge regarding the role of HDACs in HNSCC. Consequently, this review aims to summarize the existing research findings and explore the potential association between HDACs and HNSCC, offering fresh perspectives on therapeutic approaches targeting HDACs that could potentially enhance the efficacy of HNSCC treatment. Additionally, the Cancer Genome Atlas (TCGA) dataset, CPTAC, HPA, OmicShare, GeneMANIA and STRING databases are utilized to provide supplementary evidence on the differential expression of HDACs, their prognostic significance and predicting functions in HNSCC patients. Graphical Abstract

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“…Fonte: O autor Sabe-se que a resistência à quimioterapia, que ocorre após a seleção e a repopulação tumoral pelas células resistentes ao tratamento (160), ainda representa um dos principais desafios no tratamento de carcinomas de cabeça e pescoço. Apesar de pouco elucidada, essa resistência tem sido associada à presença das CTTs na população intratumoral, uma vez que, essa pequena população apresenta mecanismos de evasão/resistência (137), que lhes permite escapar da radioterapia (17) e da quimioterapia convencional (15), além de possuírem a capacidade de iniciar e manter o crescimento de uma nova população (137), favorecendo as recidivas e contribuindo para as metástases tumorais.…”

Section: Ação Dos Fármacos Sobreunclassified

Efeito de quimioterápicos inibidores de histonas deacetilases sobre células-tronco tumorais derivadas de linhagens de carcinoma mucoepidermoide de glândula salivar

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Ao meu amado avô Geraldo, meu maior exemplo de amor, resiliência, humildade e superação. Minha maior saudade! Você será, para sempre, a corda do meu coração. Obrigada por tudo e por tanto! Ao meu avô Celino e meu padrasto Amarildo, que lutaram bravamente pela vida, mas acabaram finalizando a sua jornada terrena durante o desenvolvimento deste trabalho. Sou muito grata por ter tido vocês na minha vida! Ao Henrique, meu amor, amigo e companheiro, que tem percorrido um longo caminho ao meu lado, sem nunca me deixar desistir. Obrigada por ser você e por acreditar tanto em mim. Sem você, nada disso teria sido possível! Aos meus pais, Juliano e Graça, e à minha família, por me apoiarem sempre e serem a base de sustentação dos meus sonhos! AGRADECIMENTOS Ao Professor Fabio Daumas Nunes, pela orientação, paciência e generosidade. Você é um exemplo para todos aqueles que tem a oportunidade de conviver com você. Agradeço imensamente por todo o aprendizado, gentileza e cuidado! À Professora Maria Fernanda, que se tornou, acima de tudo, uma grande amiga. Agradeço imensamente por ter apoiado a execução deste trabalho, desde o início. Você é, sem dúvidas, uma inspiração para mim. Muito obrigada pelo carinho e por me ensinar tanto. À Profª Drª Marília Trierveiler Martins, por orientar o meu processo de aprendizagem em Patologia Oral e Maxilofacial desde o início. Agradeço ainda, por compartilhar comigo toda a estrutura do Labitron, para que este trabalho fosse desenvolvido.

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Epigenetic modifications control loss of adhesion and aggressiveness of cancer stem cells derived from head and neck squamous cell carcinoma with intrinsic resistance to cisplatin

Cited by 8 publications

References 52 publications

FTY720 increases paclitaxel efficacy in cisplatin‐resistant oral squamous cell carcinoma

FTY720 increases paclitaxel efficacy in cisplatin‐resistant oral squamous cell carcinoma

Targeting histone deacetylases in head and neck squamous cell carcinoma: molecular mechanisms and therapeutic targets

Efeito de quimioterápicos inibidores de histonas deacetilases sobre células-tronco tumorais derivadas de linhagens de carcinoma mucoepidermoide de glândula salivar

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