Oral squamous cell carcinoma may originate from bone marrow-derived stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE153918 | GEO | 2020/07/08
REPOSITORIES: GEO
Similar Datasets
Project description:In this study we used in vitro approaches to investigate whether it has any inhibitory properties on OSCC cells. We also tried to understand the possible mechanisms of Sal B on this type of malignancy with respect to angiogenesis. 2 OSCC cell lines were treated with 100ug/ml Sal B for 48hours. cDNAmicroarray was used to evaluated the expressions of 96 genes known to be involving in modulating the biological process of angiogenesis.
2011-05-21 | E-GEOD-29416 | biostudies-arrayexpress
Project description:The chromosome 9p21 locus comprises several tumor suppressor genes including MTAP, CDKN2A and CDKN2B, and its homo- or heterozygous deletions are associated with reduced survival in multiple cancer types. We report that mice with germline monoallelic deletion or induced biallelic deletion of the 9p21-syntenic locus (9p21s) developed fatal myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN)-like disease associated with aberrant trabecular bone formation and/or fibrosis in the bone marrow (BM). Reciprocal BM transfers and conditional targeting of 9p21s suggested that the disease originates in the BM stroma. Single-cell analysis of 9p21s-deficient BM stroma revealed the expansion of chondrocyte and osteogenic precursors, reflected in increased osteogenic differentiation in vitro. It also showed reduced expression of factors maintaining hematopoietic stem/progenitor cells, including Cxcl12. Accordingly, 9p21s-deficient mice showed reduced levels of circulating Cxcl12 and a concomitant upregulation of the pro-fibrotic chemokine Cxcl13. Our study highlights the potential of mutations in the BM microenvironment to drive MDS/MPN-like disease. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.
2023-06-06 | GSE211779 | GEO
Project description:Hypoxic microenvironment plays important roles in the progression of solid tumors including oral squamous cell carcinoma (OSCC). Long noncoding RNAs (lncRNAs) have gained much attention in the past few years. However, it is not clear whether lncRNAs could regulate hypoxia-adaptation of OSCC, and which lncRNAs participate in this process. Using an lncRNA microarray, we analyzed the aberrant lncRNA expression profiles in OSCC tissues compared with paired normal oral mucosa as well as in hypoxic OSCC cells compared with normoxic OSCC cells. Our data revealed 2053 differentially expressed (Fold Change >= 2.0, P-value <= 0.05) lncRNAs, among which 934 lncRNAs were significantly up-regulated and 1119 lncRNAs were down-regulated in OSCC compared with paired normal mucosa. Six OSCC tissues and paired normal oral mucosa were obtained from 6 patients with OSCC. LncRNA expression profiles were evaluated by an Agilent Human LncRNA Array v3.0 (8 x 60K, Arraystar).
2016-07-26 | E-GEOD-84805 | biostudies-arrayexpress
Project description:In this study we used in vitro approaches to investigate whether it has any inhibitory properties on OSCC cells. We also tried to understand the possible mechanisms of Sal B on this type of malignancy with respect to angiogenesis.
2011-05-21 | GSE29416 | GEO
Project description:Tissue-resident stem cell senescence leads to stem cell exhaustion, which is a major cause of physiological and pathological aging. Stem cells-derived extracellular vesicles(SCs-EVs) have been reported to possess therapeutic potential in preclinical studies for diverse diseases. However, whether SCs-EVs could rejuvenate senescent tissue stem cell to prevent age-related disorders still remains unknown. Here, we showed that chronic application of human embryonic stem cells-derived extracellular vesicles (hESCs-sEVs) rescues senescent bone marrow MSCs (BM-MSCs) function and prevents age-related bone loss in aging mice. Transcriptome analysis revealed that hESCs-sEVs treatment up-regulates the expression of genes involved in anti-aging, stem cell proliferation and osteogenic differentiation in BM-MSCs. Furthermore, liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis identified 4122 proteins encapsulated in hESCs-sEVs. Bioinformatics analysis predicated that protein components in the hESCs-sEVs function in a synergistic way to induce the activation of several canonical signaling pathways, including Wnt, Sirtuin, AMPK, PTEN signaling, which results in the up-regulation of anti-aging genes in BM-MSCs and then the recovery of senescent BM-MSCs function. Collectively, our findings reveal the effect of hESCs-sEVs in reversing BM-MSCs senescence and age-related osteogenic dysfunction, and thereby preventing age-related bone loss. Given that hESCs-sEVs could alleviate senescence of tissue-resident stem cells, it might be a promising therapeutic candidate for age-related diseases.
2021-08-30 | PXD018655 | Pride
Project description:Myelodysplastic syndrome (MDS) is a group of heterogeneous clonal stem cell disorders. We hypothesize that gene expression changes in the bone marrow (BM) microenvironment might play a fundamental role in the development and progression of MDS. The goal of the present study is to investigate the differences in gene expression profiles of BM mesenchymal stromal cells (MSCs) between MDS patients and normal individuals, as well as between MDS subtypes. To this end, we applied global gene expression profiling on BM MSCs from adult de novo MDS patients and from controls. The results suggest that gene expression of the MDS BM microenvironment is difference from control BM. In particular, interferon signaling pathway was shown to be up-regulated in MDS BM. The results also showed altered expression according to disease progression. The present study provides evidence supporting MDS as an immune disease and suggests that BM MSCs are a possible therapeutic target in MDS.
2015-03-25 | GSE61853 | GEO
Project description:In the tumour microenvironment (TME), stroma components play a vital role in tumour development. Myeloid-derived suppressor cells (MDSC) recruited by tumour cells in TME support tumour development. However, the influence of stroma on MDSC is unclear. Here we aimed to unveil the roles of stroma in the recruitment of MDSC in oral squamous cell carcinoma (OSCC). We created xenograft OSCC models on GFP+ bone marrow transplanted nude mice. We co-xenografted human OSCC cells line (HSC-2) with three different types of stromal cells, including human dermal fibroblasts (HDF) or patient-derived stromal cells (PDS1 and PDS2) isolated from two OSCC patients, or without stromal cells. Tumour/stroma co-xenograft models recruited significantly higher numbers of GFP+ bone marrow (BM) cells than the tumour cells alone xenografted group. However, only patient-derived stroma xenograft (PDSX) models promoted GR1/CD11b/Arg1 triple-positive MDSC, which was the main population influenced by stromal character and depended on the stroma secreted CCL2. In vitro inhibition of CCL2 synthesis in PDS cocultures also resulted in significantly decreased migration of BM cells than in HDF coculture and HSC-2 alone culture. Moreover, CCR2+ MDSC infiltrated considerably higher in PDSX models. Taken together, we demonstrated that stromal cells are responsible for MDSC recruitment and stroma secreted CCL2 play an essential role in MDSC recruitment in OSCC.
2021-08-18 | GSE164374 | GEO
Project description:To examine the differences between bone marrow (BM) and peripheral blood (PB) myeloblasts in acute myeloid leukaemia (AML), we compared CD34+ myeloblasts of paired BM and peripheral blood (PB) samples from AML patients using microarray.
2008-09-30 | GSE12326 | GEO
Project description:HuntingtonM-bM-^@M-^Ys disease (HD) is a neurodegenerative disorder that is associated with the deposition of proteinaceous aggregates in the brains of HD patients and mouse models. Previous studies have suggested that wide-scale disruption of protein homeostasis occurs in protein folding diseases. Protein homeostasis can be maintained by activation of the heat shock response (HSR) via the transcription factor heat shock factor 1 (HSF1), the pharmacological activation of which can be achieved by Hsp90 inhibition and has been demonstrated to be beneficial in cell and invertebrate models of HD. Whether the HSR is functional in HD and whether its activation has therapeutic potential in mammalian HD models is currently unknown. To address these issues, we used a novel, brain penetrant Hsp90 inhibitor to activate the HSR in brain after systemic administration. Microarrays, quantitative PCR and western blotting showed that the HSR becomes impaired with disease progression in two mouse models of HD and that this originates at the level of transcription. HuntingtonM-bM-^@M-^Ys disease (HD) is a neurodegenerative disorder that is associated with the deposition of proteinaceous aggregates in the brains of HD patients and mouse models. Previous studies have suggested that wide-scale disruption of protein homeostasis occurs in protein folding diseases. Protein homeostasis can be maintained by activation of the heat shock response (HSR) via the transcription factor heat shock factor 1 (HSF1), the pharmacological activation of which can be achieved by Hsp90 inhibition and has been demonstrated to be beneficial in cell and invertebrate models of HD. Whether the HSR is functional in HD and whether its activation has therapeutic potential in mammalian HD models is currently unknown. To address these issues, we used a novel, brain penetrant Hsp90 inhibitor to activate the HSR in brain after systemic administration. Microarrays, quantitative PCR and western blotting showed that the HSR becomes impaired with disease progression in two mouse models of HD and that this originates at the level of transcription. mRNA expression analysis was performed by microarray in 12 week old R6/2 and WT mice treated with vehicle or HSP990 for 4h (12mg/kg).The following number of replicates was analysed for each genotype: 7 for WT+vehicle, 10 for WT+HSP990, 7 for R6/2+vehicle and 8 for R6/2+HSP990. Microarray quality control was performed using the software package provided on RACE (http://race.unil.ch).
2014-06-01 | E-GEOD-29681 | biostudies-arrayexpress
Project description:OSCC is associated with substantial mortality and morbidity. In this study, we built on our previous molecular work to identify and validate a prognostic 13-gene signature that showed a higher ability than tumor stage in predicting survival for patients with HPV-negative oral squamous cell carcinoma (OSCC). We previously reported 131 genes to be associated with survival in OSCC patients. In this study, we applied L1/L2-penalized Cox regression models to the Affymetrix array data from 97 HPV-negative OSCC patients on the 131 gene to identify a model for prediction of OSCC-specific survival. We then tested the model in an independent dataset and compared to tumor stage.
2013-03-07 | E-GEOD-41613 | biostudies-arrayexpress