Similar Datasets
Project description:The RNA-seq study of CCL20 in OSCC cell line
| PRJNA1035051 | ENA
Project description:This study aimed to explore the underlying molecular mechanism of REEP6 in OSCC progression. REEP6 plays a role in cellular ferroptosis.
2024-11-20 | GSE271159 | GEO
Project description:Oral squamous cell carcinoma (OSCC) is a main reason of oral cancer mortality and morbidity. Cancer of oral cavity in central south Asia, ranks among third most common kinds of cancer. The discovery of candidate markers to differentiate normal from malignant cells in clinical diagnosis of OSCC would be of critical importance because this malignancy has poor prognosis. To improve the clinical outcome in OSCC patients, the present study was aimed at identifying robust candidate biomarkers for early OSCC diagnosis and to enhance understanding of the mechanisms of disease progression and pathogenesis. Of particular interest are proteins that can be found in tissue lysates of OSCC tumor vs normal adjacent mucosa samples and secreted in cell line Secretomes of HNSCC for non-invasive detection. We analysed 17 paired human malignant OSCC tissues and normal adjacent tissue in addition to secretomes of 9 HNSCC cell lines. The proteome dataset of OSCC and normal tissues consisted of 5,123 protein groups, including 299 proteins with strong differential expression (p-value <0.01, fold change barrier to ˃+2 and <-2, 205 upregulated and 94 down regulated) and 134 common proteins were also found out of total dataset of 4473 identified proteins of HNSCC cell line secretomes. Functional data analysis revealed that these differential proteins were significantly associated with multiple biological processes. Myogenesis, Fatty Acid Metabolism and KRAS Signaling DN were associated with the proteins downregulated in cancer tissues, while Protein Secretion, Unfolded Protein Response, Spliceosomal complex assembly, Protein localization to endosome and Interferon Gamma Response were enriched in the set of upregulated proteins and these regulated proteins may be classically or non-classically secreted. Furthermore, we found differential enrichment of Creb3L1, ESRRA, YY, ELF2, STAT1 and XBP transcription factors potentially regulating these major pathways.
2022-04-04 | PXD025701 | Pride
Project description:Recent reports have revealed that EMT is involved in cancer invasion and progression including oral squamous cell carcinoma (OSCC). Previously, we have also studied on the association of p63 gene, a homolog of the p53 tumor suppressor gene, with EMT in OSCC cells. Furthermore, we also demonstrated that down-regulation of ΔNp63 accompanied with EMT and that re-expression of ΔNp63β by stable cDNA transfection in OSCC cell lines reverted the EMT phenotype. However, the detail mechanisms of ΔNp63β-mediated EMT remain to be unclear. Recent studies have shown that several microRNAs (miRNAs) are also involved in EMT process of human cancer by targeting EMT-related transcription factors. We thus sought to identify responsible miRNA associated with ΔNp63β-mediated EMT using miRNA microarray analyses.
2017-06-01 | GSE94047 | 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: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 microarray also identified 942 lncRNAs that were up-regulated and 507 lncRNAs that were down-regulated in cells cultured under hypoxia compared with those cultured under normoxia (Fold Change >= 2.0, P-value <= 0.05). An OSCC cell line Cal-27 was cultured under either 20% O2 (normoxic) or 1% O2 (hypoxic) conditions. Three samples from each group were obtained for microarray study.
2016-07-26 | E-GEOD-84790 | biostudies-arrayexpress
Project description:LIX1L stabilization of CCL20 promotes fibrosis
| PRJNA550026 | ENA
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.
2016-07-26 | GSE84805 | GEO
Project description:Oral Squamous Cell Carcinoma (OSCC) is a type of cancer that arises from preneoplastic precursors, which undergo genetic and epigenetic modifications. Lysine-specific demethylase 1 (LSD1) is a key OSCC promoter. LSD1 knockout or pharmacological inhibition in mouse OSCC reversed OSCC preneoplasia in our study. LSD1 inhibition attenuated the cell cycle, immunosuppression and promoted the infiltration of CD45+, TCRß+, CD4+, and CD8+ cells. Next, we tested the clinical candidate LSD1 inhibitor (Seclidemstat) in feline clinically spontaneous natural OSCC and found that it was safe and attenuated the STAT3 network. Mechanistic studies have shown that LSD1 reprograms preneoplasia to promote STAT3 signaling, cell cycle mediator CDK7, and immunosuppressive CTLA4 to OSCC progression. Interestingly, we found that the LSD1 inhibitor (SP2509) attenuated cyclin-dependent kinase 7 (CDK7) phosphorylation at T170 and eukaryotic initiation factor 4 B (Eif4B) phosphorylation at S422. We identified a new mechanism in OSCC preneoplasia that LSD1 promotes STAT3 mediated by CDK7 phosphorylation, leading to overall changes in the tumor microenvironment, leading to immunosuppression and progression to OSCC, which could have applications for understanding the mechanism as well as design strategies to control the progression of preneoplasia to OSCC.
2025-04-23 | GSE277930 | GEO
Project description:Oral Squamous Cell Carcinoma (OSCC) is a type of cancer that arises from preneoplastic precursors, which undergo genetic and epigenetic modifications. Lysine-specific demethylase 1 (LSD1) is a key OSCC promoter. LSD1 knockout or pharmacological inhibition in mouse OSCC reversed OSCC preneoplasia in our study. LSD1 inhibition attenuated the cell cycle, immunosuppression and promoted the infiltration of CD45+, TCRß+, CD4+, and CD8+ cells. Next, we tested the clinical candidate LSD1 inhibitor (Seclidemstat) in feline clinically spontaneous natural OSCC and found that it was safe and attenuated the STAT3 network. Mechanistic studies have shown that LSD1 reprograms preneoplasia to promote STAT3 signaling, cell cycle mediator CDK7, and immunosuppressive CTLA4 to OSCC progression. Interestingly, we found that the LSD1 inhibitor (SP2509) attenuated cyclin-dependent kinase 7 (CDK7) phosphorylation at T170 and eukaryotic initiation factor 4 B (Eif4B) phosphorylation at S422. We identified a new mechanism in OSCC preneoplasia that LSD1 promotes STAT3 mediated by CDK7 phosphorylation, leading to overall changes in the tumor microenvironment, leading to immunosuppression and progression to OSCC, which could have applications for understanding the mechanism as well as design strategies to control the progression of preneoplasia to OSCC.
2025-04-23 | GSE277935 | GEO