Oral cancer stem cell Biology
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB52288 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9592690_1.fastq.gz | Fastqsanger.gz | |||
| ERR9592690_2.fastq.gz | Fastqsanger.gz | |||
| ERR9592691_1.fastq.gz | Fastqsanger.gz | |||
| ERR9592691_2.fastq.gz | Fastqsanger.gz | |||
| ERR9592692_1.fastq.gz | Fastqsanger.gz |
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Project description:<h4>Background</h4>Cancer metabolism is emerging as an important focus area in cancer research. However, the in vitro cell culture conditions under which much cellular metabolism research is performed differ drastically from in vivo tumor conditions, which are characterized by variations in the levels of oxygen, nutrients like glucose, and other molecules like chemotherapeutics. Moreover, it is important to know how the diverse cell types in a tumor, including cancer stem cells that are believed to be a major cause of cancer recurrence, respond to these variations. Here, in vitro environmental perturbations designed to mimic different aspects of the in vivo environment were used to characterize how an ovarian cancer cell line and its derived, isogenic cancer stem cells metabolically respond to environmental cues.<h4>Results</h4>Mass spectrometry was used to profile metabolite levels in response to in vitro environmental perturbations. Docetaxel, the chemotherapeutic used for this experiment, caused significant metabolic changes in amino acid and carbohydrate metabolism in ovarian cancer cells, but had virtually no metabolic effect on isogenic ovarian cancer stem cells. Glucose deprivation, hypoxia, and the combination thereof altered ovarian cancer cell and cancer stem cell metabolism to varying extents for the two cell types. Hypoxia had a much larger effect on ovarian cancer cell metabolism, while glucose deprivation had a greater effect on ovarian cancer stem cell metabolism. Core metabolites and pathways affected by these perturbations were identified, along with pathways that were unique to cell types or perturbations.<h4>Conclusions</h4>The metabolic responses of an ovarian cancer cell line and its derived isogenic cancer stem cells differ greatly under most conditions, suggesting that these two cell types may behave quite differently in an in vivo tumor microenvironment. While cancer metabolism and cancer stem cells are each promising potential therapeutic targets, such varied behaviors in vivo would need to be considered in the design and early testing of such treatments.
2021-11-05 | MTBLS150 | MetaboLights
Project description:An investigation of canine oral squamous cell carcinomas
2024-06-30 | PRJEB77007 | EVA
Project description:Purpose: Previously, we have reported the effectiveness of elemental diet (ED) Elental® against radiotherapy- or chemoradiotherapy- induced oral mucositis (Support Care Cancer 2016, Mol Clin Oncol 2019). However, administration of additional nutrition or ED in oral cancer patients might also provide extra nutrition for cancer cells, which could result in cancer development. At present, it is still unclear whether the beneficial effect of ED can be expected to surpass its possible harmful effect on oral cancer treatment. In the present study, we tried to clarify whether Elental® has different effects on human oral keratinocyte (HOK) cells compared to oral squamous cell carcinoma (OSCC) cells (HSC2). Method: Gene expression profiles of HOK cells and HSC2 cells treated with Elental® were generated by deep sequencing. Results: Whole transcriptome analysis data suggested that Elental® helped in the proliferation and survival of HOK through the induction of ERK. Moreover, Elental® added stress to HSC2 through the induction of endoplasmic reticulum stress response marker, BiP. Our results showed that Elental® might add stress to HSC2, and provide growth stimulation to HOK. Conclusion: Whole transcriptome analysis showed different gene expression profile between HOK cells and HSC2 cells treated with Elental®, suggesting that effects of Elental® might differ between normal oral cells and oral cancer cells.
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Project description:RNAseq analysis of oral cancer and oral leukoplakia patients. Oral biopsies from 37 patients were obtained for sequencing using RNAseq including control, oral leukoplakia patients and oral cancer patients.
2022-10-08 | E-MTAB-12205 | biostudies-arrayexpress
Project description:RATIONALE: Peripheral stem cell transplantation may be able to replace immune cells that were destroyed by chemotherapy and radiation therapy used to kill tumor cells.
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Project description:iTRAQ-based comparison of proteins derived from oral cells collected by brush biopsy. Protein abundance levels compared between oral pre-malignant cells, oral cancer cells and healthy normal cells, all collected from human patients. Two separate iTRAQ labeled biological replicate analyses were conducted.
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Project description:micro-RNA in cancer-associated fibroblasts in oral squamous cell carcinoma vs. dysplasia-associated fibroblasts from dysplastic oral lesions vs. normal fibroblasts from normal oral mucosa from healthy individual.
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Project description:Gene expression of mouse oral cancer cell lines
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Project description:A comparative microarray analysis of indolent or aggressive mouse oral cancer cell lines was performed to identify gene expression signatures and specific molecules involved in aggressive tumor growth. We compared 3 indolent cell lines (MOC1, MOC22, MOC23) to 1 aggressive line and it's derivatives (MOC2, MOC2-7 and MOC2-10). We also included a cell line generated from a lymph node metastasis of the MOC2 tumor. The lines were all analyzed in triplicated except for MOC1 which was done in quadruplicate. Finally, we included duplicate samples of primary, normal C57BL/6 oral keratinocytes grown in the same media as the MOC cell lines.
2014-04-13 | E-GEOD-50041 | 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 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