KLK6-related gene expression profile in FaDu cells
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PROVIDER: PRJNA505264 | ENA |
REPOSITORIES: ENA
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Project description:Epithelial-to-mesenchymal transition (EMT) is a dynamic process and critically contributes to treatment resistance, cancer cell dissemination and metastasis. Main objective of this study was to investigate the functional interaction between Kallikrein-related peptidase 6 (KLK6) and aldehyde dehydrogenase 1A (ALDH1A)-related retinoic acid (RA) signaling as recent studies reported their impact on molecular features resembling EMT in several malignancies, including head and neck squamous cell carcinoma (HNSCC). In HNSCC cell lines, we demonstrate that KLK6 is not only a downstream target of ALDH1A-related RA signaling, but also acts as an upstream regulator of ALDH1A3 expression. KLK6 and ALDH1A3 co-expression was confirmed in a mouse xenograft model and two independent HNSCC cohorts (HIPO-HNC and TCGA-HNC). KLK6 and ALDH1A3 co-expressed genes in HNSCC, which are also differentially expression in HNSCC cells with silenced KLK6 expression unraveled several subgroups of HNSCC patients with distinct histopathological and clinical features. In summary, our study highlights a new functional circuit with KLK6 and ALDH1A3 as key nodes and unraveled a gene expression signature, which predicts unfavorable prognosis in human papilloma virus (HPV)-negative HNSCC.
2021-11-01 | GSE122448 | GEO
Project description:FaDu cells were infected with lentivirus containing sh-luciferase plasmid to compared with cells infected with sh-G9a containing lentivirus. We performed microarray analysis to identify the genes possibly regulated by G9a in FaDu cells
2017-02-13 | GSE56330 | GEO
Project description:Differential gene expression analysis of FaDu cells overexpressing TINCR-HA-FLAG or an empty vector.
2024-07-16 | GSE180301 | GEO
Project description:To screen the genes regulated by wt-Snail and non-acetylated Snail The successful development of cancer metastasis requires two major events: the reprogramming of cancer cells to increase their migration and tumor-initiation capabilities; and the remodeling of the tumor microenvironment to facilitate invasion and colonization of cancer cells. Epithelial-mesenchymal transition (EMT) is a crucial mechanism for reprogramming cancer cells to possess tumor initiation and migration capabilities1,2. However, the role of EMT in the interplay between tumor and host cells is largely unknown. The EMT regulator Snail is mainly known as a transcriptional repressor of the adhesion protein E-cadherin, whose repression is considered to be a key step in initiating metastasis3,4. We previously found that Snail can also act as an activator that induces the transcription of ERCC15 and IL86. Here we show that Snail is acetylated by CREB-binding protein (CBP) and that Snail and CBP co-occupy the promoters of target genes to activate transcription of the target genes. Furthermore, Snail activates the expression of a panel of cytokine genes, including TNFa (which forms a positive feedback loop with Snail to amplify the signal) and CCL2 and CCL5 (which facilitate the recruitment of macrophages by cancer cells). Our results demonstrate a novel function for Snail, providing new understanding of the recruitment of host cells to tumor sites during metastatic evolution. Establish stable transfectants of pCDH-Snail and pCDH-Snail2R in FaDu cells and analyze the mRNA expression level of by cDNA microarray. FaDu transfected with pCDH vector was used as a control experiment.
2014-08-16 | E-GEOD-58592 | biostudies-arrayexpress
Project description:Gene expression profiling of FaDu cells overexpressing TINCR-HA-FLAG
| PRJNA747713 | ENA
Project description:Expression of HIF-1a or Twist1 or Bmi1 in human hypopharyngeal cancer cell line FADU results in the drift of transcriptome profile from an epithelial cell-like signature to a mesenchymal stem cell-like signature. Stable transfection of pHA-HIF1a(dODD), pFLAG-Twist1 or pcDNA3-Bmi1 in FADU cell and analyzed the transcriptome by cDNA microarray. FADU transfected with pcDNA3.1 empty vector was used as a control of experiment.
2010-12-10 | E-GEOD-19406 | biostudies-arrayexpress
Project description:Microarray analyses for the identification of differences in gene expression patterns have increased our understanding of the molecular mechanism of ARID3B in HNSCC.We used gene expression analysis data from FaDu-ARID3B and FaDu-pCDH to identify differentially expressed probes. The expression of the embryonic stem cell (ESC) signature in cancer cells indicates the coordinated regulation of the stemness genes in cancer stem cells, which are responsible for cancer initiation and dissemination. let-7 family microRNAs are crucial regulators for stem cell differentiation. In cancer cells, let-7 suppresses cancer stemness through targeting different oncogenes such as c-Myc, RAS, and HMGA2. However, most let-7 target genes are oncogenes rather than stemness factors, and the mechanism of let-7-repressed stemness is unclear. Here we demonstrate that let-7 supresses the formation of AT-rich interacting domain 3B (ARID3B) complex through targeting the expression of ARID3B, the interacting partner ARID3A, and importin 9. ARID3B complex recruits histone demethylase 4C (KDM4C) to the regulatory region of stemness genes for reducing histone 3 lysine 9 trimethylation, resulting in an open configuration of the chromatin of stemness genes. In cancer tissues, ARID3B expression correlates with the nuclear ARID3A expression and a worse prognosis. This result highlights the role of let-7 in regulating stemness through histone modifications.
2015-12-01 | GSE66602 | GEO
Project description:CRISPR-Cas9 screen of FaDu Cas9 cells treated with fractionated RT.
2021-03-07 | GSE147084 | GEO
Project description:RNA-Seq of FaDu Cas9 isogenic cells treated with fractionated RT.
2021-03-07 | GSE147085 | GEO
Project description:Expression of HIF-1a or Twist1 or Bmi1 in human hypopharyngeal cancer cell line FADU results in the drift of transcriptome profile from an epithelial cell-like signature to a mesenchymal stem cell-like signature.
2010-12-10 | GSE19406 | GEO