Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA300868 | ENA |
REPOSITORIES: ENA
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Project description:Phenotypic plasticity determines cancer stem cell therapeutic resistance in oral squamous cell carcinoma I
| PRJNA300869 | ENA
Project description:Cancer stem cells (CSCs) drive tumour spread and therapeutic resistance, and can undergo epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) to switch between epithelial and post-EMT sub-populations. Examining oral squamous cell carcinoma (OSCC), we now show that increased phenotypic plasticity, the ability to undergo EMT/MET, underlies increased CSC therapeutic resistance within both the epithelial and post-EMT sub-populations. The post-EMT CSCs that possess plasticity exhibit particularly enhanced therapeutic resistance and are defined by a CD44highEpCAMlow/-CD24+ cell surface marker profile. Treatment with TGFβ and retinoic acid (RA) enabled enrichment of this sub-population for therapeutic testing, through which the endoplasmic reticulum (ER) stressor and autophagy inhibitor Thapsigargin was shown to selectively target these cells. Demonstration of the link between phenotypic plasticity and therapeutic resistance, and development of an in vitro method for enrichment of a highly resistant CSC sub-population, provides an opportunity for the development of improved chemotherapeutic agents that can eliminate CSCs. The CA1 OSCC cell line was sub-cloned to derive 4 clonal sub-lines, termed pEMT-P, pEMT-S, Epi-S and Epi-P (here 18, 23, 7 and 4 respectively).
2016-01-12 | E-GEOD-74578 | biostudies-arrayexpress
Project description:Cancer stem cells (CSCs) drive tumour spread and therapeutic resistance, and can undergo epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) to switch between epithelial and post-EMT sub-populations. Examining oral squamous cell carcinoma (OSCC), we now show that increased phenotypic plasticity, the ability to undergo EMT/MET, underlies increased CSC therapeutic resistance within both the epithelial and post-EMT sub-populations. The post-EMT CSCs that possess plasticity exhibit particularly enhanced therapeutic resistance and are defined by a CD44highEpCAMlow/-CD24+ cell surface marker profile. Treatment with TGFβ and retinoic acid (RA) enabled enrichment of this sub-population for therapeutic testing, through which the endoplasmic reticulum (ER) stressor and autophagy inhibitor Thapsigargin was shown to selectively target these cells. Demonstration of the link between phenotypic plasticity and therapeutic resistance, and development of an in vitro method for enrichment of a highly resistant CSC sub-population, provides an opportunity for the development of improved chemotherapeutic agents that can eliminate CSCs. The clonal derivative of the CA1 OSCC cell line termed 18 here (otherwise termed pEMT-P) was treated with 0.5ng/ml TGFbeta and/or 5uM RA for eight days, with media changed every second day. The LM OSCC cell line was FACS sorted to recover the CD44highEpCAMlowCD24+ sub-population, which was then treated with 0.5ng/ml TGFbeta and/or 5uM RA for eight days, with media changed every second day. The parental CA1 and LM cell lines are included as reference samples.
2016-01-12 | E-GEOD-74580 | biostudies-arrayexpress
Project description:Cancer stem cells (CSCs) drive tumour spread and therapeutic resistance, and can undergo epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) to switch between epithelial and post-EMT sub-populations. Examining oral squamous cell carcinoma (OSCC), we now show that increased phenotypic plasticity, the ability to undergo EMT/MET, underlies increased CSC therapeutic resistance within both the epithelial and post-EMT sub-populations. The post-EMT CSCs that possess plasticity exhibit particularly enhanced therapeutic resistance and are defined by a CD44highEpCAMlow/-CD24+ cell surface marker profile. Treatment with TGFβ and retinoic acid (RA) enabled enrichment of this sub-population for therapeutic testing, through which the endoplasmic reticulum (ER) stressor and autophagy inhibitor Thapsigargin was shown to selectively target these cells. Demonstration of the link between phenotypic plasticity and therapeutic resistance, and development of an in vitro method for enrichment of a highly resistant CSC sub-population, provides an opportunity for the development of improved chemotherapeutic agents that can eliminate CSCs.
2016-01-12 | GSE74580 | GEO
Project description:Cancer stem cells (CSCs) drive tumour spread and therapeutic resistance, and can undergo epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) to switch between epithelial and post-EMT sub-populations. Examining oral squamous cell carcinoma (OSCC), we now show that increased phenotypic plasticity, the ability to undergo EMT/MET, underlies increased CSC therapeutic resistance within both the epithelial and post-EMT sub-populations. The post-EMT CSCs that possess plasticity exhibit particularly enhanced therapeutic resistance and are defined by a CD44highEpCAMlow/-CD24+ cell surface marker profile. Treatment with TGFβ and retinoic acid (RA) enabled enrichment of this sub-population for therapeutic testing, through which the endoplasmic reticulum (ER) stressor and autophagy inhibitor Thapsigargin was shown to selectively target these cells. Demonstration of the link between phenotypic plasticity and therapeutic resistance, and development of an in vitro method for enrichment of a highly resistant CSC sub-population, provides an opportunity for the development of improved chemotherapeutic agents that can eliminate CSCs.
2016-01-12 | GSE74578 | GEO
Project description:Identification of CMTM6 as a novel mediator of cisplatin resistance in oral squamous cell carcinoma
2020-01-07 | MSV000084761 | MassIVE
Project description:Common overexpressing genes were identified in all human oral squamous cell carcinoma tissues and/or cultured cells. Ten oral squamous cell carcinoma tissues and 10 human oral squamous cell carcinoma cell lines were analyzed. Three normal oral mucosa tissues and a human non-neoplastic keratinocyte cell lines were used as control samples.
2012-09-30 | E-GEOD-36090 | biostudies-arrayexpress
Project description:The hypoxic tumor microenvironment (TME) is a common hallmark of solid cancers, including oral squamous cell carcinoma (OSCC). Hypoxia is predominantly regulated by the hypoxia-inducible factor-1 alpha (HIF-1α) and can alter the histone acetylation and methylation profile involved in drug resistance and possible therapeutic options for solid cancer. Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor (HDACi) that targets HIF-1α stability, whereas PX-12 (1-methylpropyl 2-imidazolyl disulfide) is a thioredoxin-1 (Trx-1) inhibitor that prevents HIF-1α accumulation. Although HDACi are efficient in cancer treatment, they are accompanied by several adverse effects and increased resistance. This can be averted by combining HDACi with a Trx-1 inhibitor, as both inhibitors are connected by interlinked inhibitory pathways. HDACi inhibit Trx-1, leading to elevated reactive oxygen species (ROS) formation and death in cancerous cells; consequently, utilizing a Trx-1 inhibitor can boost the efficacy of HDACi. Previously, we investigated a synergistic interaction between vorinostat and PX-12 in an oral squamous carcinoma (OSCC) cell line under hypoxia. Here, we report to determine the effect of both inhibitors on histone acetylation and methylation expression levels under hypoxia in the CAL 27 cell line using mass spectrometry. We found several crucial histone marks, such as H3K4me1, H3K9ac, H3K9me, H3K14ac, H3K27me, H3K36me, H4K12Ac, and H4K16ac. The global analysis for histone acetylation and methylation and on specific residue shows their expression level was altered differentially by individual and combined inhibitor treatment. Our results provide an implication to investigate the underlying epigenetic mechanisms of histone acetylation and methylation levels in oral squamous cell carcinoma for a better understanding of developing drugs for cancer therapy.
2025-05-07 | PXD053244 | Pride
Project description:Aberrant upregulation of a single oncogene FOXM1 in primary normal human oral epithelial cells orchestrated a cancer-like methylome landscape This study have identified a unique FOXM1-induced epigenetic signature which may have potentials as biomarkers for early oral cancer screening, diagnostic and/or therapeutic interventions Comparisons of primary human normal oral keratinocytes transduced with either EGFP (control) or FOXM1B and a head and neck squamous cell carcinoma cell line SCC15
2012-04-18 | E-GEOD-31767 | biostudies-arrayexpress
Project description:Predictive Value of MicroRNAs in the Progression of Oral Leukoplakias Comparison of 10 samples from non-progressive leukoplakias (did not turn into oral squamous cell carcinoma), with 10 samples from progressive leukoplakias (turned into oral squamous cell carcinoma w/in 5 yrs)
2015-02-01 | E-GEOD-62809 | biostudies-arrayexpress