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GSE153918
Homo sapiens
16 Downloadable Samples
Affymetrix Human Genome U219 Array (hgu219)
Description
In this study, sex chromosome analysis was performed in patients with oral squamous cell carcinoma (OSCC) that developed after hematopoietic stem cell transplantation from the opposite gender to examine whether OSCC originates from bone marrow (BM) stem cells. Gene expression patterns in patients with possible BM stem cell-derived OSCC were compared with those in patients with normally developed OSCC.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
Objective. A variety of chemokines contribute the pathogenesis of Sjgrens syndrome (SS). However, the comprehensive analysis as for clinically potent ckemokines in SS has not been performed. In this study, focusing on CXC chemokines, we investigated the precise molecular mechanism and the clinical significance through chemokine and its receptor in the autoimmune lesions of primary SS. Methods. Gene expression profiles in the lip salivary glands (LSGs) from pSS patients and controls were analyzed using DNA microarray. Expression of chemokines and their receptor of biopsy samples of pSS pathients and controls were detected by immunofluorescence analysis. In addition, in vitro experiments using human salivary gland ductal and acinar cell lines were performed to analyze the expression of chemokines and signaling pathwaycytokines by qRT-PCR, ELISA, and Western blot analysis. Results. Gene expression profiles and immunohistochemical analysis revealed that IFN--induced CXCL9 and CXCL10 were significantly increased in LSGs of pSS patients. In vitro experiments revealed that the protein expression of CXCL10 in ductal and acinar cells was differentially regulated by IFN- or TNF- via NF-B or JAK/STAT pathway. Moreover, CXCR3 expression was detected mainly in CD68+ macrophages, CD123+ plasmacytoid dendritic cells (pDCs), and in a few CD3+ T cells. Finally, Spearman's rank analysis revealed a negative correlation between the existence of CXCR3+ cells and pathological grading in LSG tissues of pSS patients (r: -0.019, p<0.01). Conclusion. These results suggest that CXCL10/CXCR3 axis plays in a key role in autoimmune response by interaction between immune cells and target cells in the pathogenesis of pSS.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Liver dysfunction and cirrhosis affect vasculature in several organ systems and cause impairment of organ functions, thereby increasing morbidity and mortality. If a mouse model of hepatopulmonary syndrome (HPS) could be established, greater insight into the genetic basis of the disease would be gained. Our objectives were to establish a mouse model of lung injury after common bile duct ligation (CBDL) and to investigate pulmonary pathogenesis for application in future therapeutic approaches. Balb/c mice were subjected to CBDL. Immunohistochemical analyses and real-time quantitative reverse transcriptional polymerase chain reaction were performed on pulmonary tissues. The presence of HPS markers were detected by western blot and microarray analyses. We observed extensive proliferation of CD31-positive pulmonary vascular endothelial cells 2 weeks after CBDL, and identified 11 up-regulated and 8 down-regulated proteins that were associated with angiogenesis. MMP-9 protein was highly expressed at 3 weeks after CBDL, and less expressed in lungs of the control group. Contrary to our expectation, lung pathology in our mouse model exhibited differences from that of rat models, and the mechanisms responsible for these differences are unknown. This phenomenon may be explained by contrasting processes related to TNF induction of angiogenic signaling pathways in the inflammatory phase; thus, we suggest that our mouse model can be applied to pulmonary pathological analyses in the inflammatory phase, i.e., to systemic inflammatory response syndrome, acute lung injury, and MOD syndrome.
Publication Title
No associated publication
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
Knockdown of Akt1 markedly inhibited the growth of GFP-SAS cells.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
SASL1 is highly metastatic to lymph nodes. ACC2 is not metastatic. We compared gene expression on cultured cells to identify genes associated to metastatic spread patterns.
Publication Title
Premetastatic vasculogenesis in oral squamous cell carcinoma xenograft-draining lymph nodes.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
Inhibition of miR-361-3p by locked nucleic acid (LNA)/DNA antisense oligonucleotide markedly suppressed the growth of GFP-SAS cells.
Publication Title
MicroRNA-361-3p is a potent therapeutic target for oral squamous cell carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations have shown a dramatic response to EGFR inhibitors (EGFR-TKI). EGFR T790M mutation and MET amplification have been recognized as major mechanisms of acquired resistance to EGFR-TKI. Therefore, MET inhibitors have recently been used in NSCLC patients in clinical trials. In this study, we tried to identify the mechanism of acquired resistance to MET inhibitor. We analyzed the antitumor effects of two MET inhibitors, PHA-665752 and crizotinib, in 10 NSCLC cell lines. EBC1 cells with MET amplification were the only cells that were sensitive to both MET inhibitors. We established PHA-665752-resistant EBC1 cells, namely EBC1-R cells. EBC1-R cells showed overexpression of ATP-binding cassette sub-family B member 1 (ABCB1) as well as phosphorylation of MET. EBC1-R cells grew as cell spheres that exhibited cancer stem cell-like (CSC) properties and epithelial mesenchymal transition (EMT). The levels of two miRNAs, miR-374a and miR-138 which targeted ABCB1, were decreased in EBC1-R cells. ABCB1 siRNA and ABCB1 inhibitor elacridar could reduce sphere numbers and suppress EMT. Elacridar could also reverse the resistance to PHA-665752 in EBC1-R cells. Our study demonstrated that ABCB1 overexpression which was associated with CSC properties and EMT was involved in the acquired resistance to MET inhibitor. Inhibition of ABCB1 might be a novel therapeutic strategy for NSCLC patients with acquired resistance to MET inhibitor.
Publication Title
Inhibition of ABCB1 Overcomes Cancer Stem Cell-like Properties and Acquired Resistance to MET Inhibitors in Non-Small Cell Lung Cancer.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Estrogens are well known steroid hormones necessary to maintain bone health. In addition, mechanical loading, which estrogen signaling may intersect with the Wnt/-catenin pathway, is also essential for bone health. As osteocytes are known as the major mechanosensory cells embedded in mineralized bone matrix, osteocyte ER deletion mice (EROcy/Ocy) were generated by mating ER floxed mice with Dmp1-Cre mice to determine functions of ER in osteocytes. Trabecular bone mineral density of female, but not male EROcy/Ocy mice was significantly decreased. Bone formation parameters in EROcy/Ocy were significantly decreased while osteoclast parameters were unchanged. This suggests that ER in osteocytes exerts osteoprotective function by positively controlling bone formation. To identify potential targets of ER, gene array analysis of Dmp1-GFP osteocytes FACS sorted from EROcy/Ocy and control mice was performed. Expression of Mdk and Sostdc1, both known inhibitors of Wnt, were significantly increased without alteration of the mature osteocyte marker Sost or -catenin. Hindlimb unloading exacerbated the trabecular bone loss, but surprisingly cortical bone was resistant. These studies show that ER in osteocytes has osteoprotective effects in trabecular bone through regulating expression of Wnt antagonists, but conversely plays a negative role in cortical bone loss due to unloading.
Publication Title
Estrogen receptor α in osteocytes regulates trabecular bone formation in female mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
Knockdown of AURKA by siAURKA and treatment with MLN8237 markedly inhibit the growth of GFP-SAS cells. We investigated the molecular mechanisms of siAURKA and MLN8237 using the Affymetrix GeneAtlasTM System.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 110 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The purpose of the present study was to investigate the association of glutathione S-transferase P1 (GSTP1) expression with resistance to neoadjuvant paclitaxel followed by 5-fluorouracil/epirubicin/cyclophosphamide (P-FEC) in human breast cancers. The relationship of GSTP1 expression and GSTP1 promoter hypermethylation with intrinsic subtypes was also investigated. In this study, primary breast cancer patients (n = 123, stage II-III) treated with neoadjuvant P-FEC were analyzed. Tumor samples were obtained by vacuum-assisted core biopsy before P-FEC. GSTP1 expression was determined using immunohistochemistry, GSTP1 promoter methylation index (MI) using bisulfite methylation assay and intrinsic subtypes using DNA microarray. The pathological complete response (pCR) rate was significantly higher in GSTP1-negative tumors (80.0%) than GSTP1-positive tumors (30.6%) (P = 0.009) among estrogen receptor (ER)-negative tumors but not among ER-positive tumors (P = 0.267). Multivariate analysis showed that GSTP1 was the only predictive factor for pCR (P = 0.013) among ER-negative tumors. Luminal A, luminal B and HER2-enriched tumors showed a significantly lower GSTP1 positivity than basal-like tumors (P = 0.002, P < 0.001 and P = 0.009, respectively), while luminal A, luminal B and HER2-enriched tumors showed a higher GSTP1 MI than basal-like tumors (P = 0.076, P < 0.001 and P < 0.001, respectively). In conclusion, these results suggest the possibility that GSTP1 expression can predict pathological response to P-FEC in ER-negative tumors but not in ER-positive tumors. Additionally, GSTP1 promoter hypermethylation might be implicated more importantly in the pathogenesis of luminal A, luminal B and HER2-enriched tumors than basal-like tumors.
Publication Title
GSTP1 expression predicts poor pathological complete response to neoadjuvant chemotherapy in ER-negative breast cancer.
Sample Metadata Fields
Age, Specimen part, Disease stage
View Samples