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Loss of SOX2 expression induces cell migration via Vimentin up-regulation and serves as unfavourable risk factor for poor survival of head and neck squamous cell carcinoma patients

ABSTRACT: Transcriptional profiling of patient derived HNSCC (head and neck squamous cell carcinoma) cell line HNO223 comparing control cells transfected with shRNA against luciferase (shLuci) with cells transfected with two different shRNAs targeting SOX2. The goal was to determine the effects of SOX2 knockdown on global gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE61599 | GEO | 2014/09/23

SECONDARY ACCESSION(S): PRJNA261666

REPOSITORIES: GEO

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Loss of SOX2 expression induces cell migration via Vimentin up-regulation and serves as unfavourable risk factor for poor survival of head and neck squamous cell carcinoma patients

Project description:Transcriptional profiling of patient derived HNSCC (head and neck squamous cell carcinoma) cell line HNO223 comparing control cells transfected with shRNA against luciferase (shLuci) with cells transfected with two different shRNAs targeting SOX2. The goal was to determine the effects of SOX2 knockdown on global gene expression. Total RNA was extracted from stably transfected HNSCC cells with shLuci (control) and two different SOX2 shRNAs (shSOX2#1 and shSOX2#2), comparing the control with each of the two SOX2 shRNAs (replicate1: shLuci vs. shSOX2#1 and replicate2: shLuci vs. shSOX2#2). The biological replicates were from two independent transfection experiments (transfection 1 and transfection 2). Gene expression profiling was performed using the Human GE 4x44K v2 Microarray according to manufacturer`s instructions (Agilent, Santa Clara, CA).

2014-09-23 | E-GEOD-61599 | biostudies-arrayexpress

Dual knockdown of Esrrb and Sox2 in mouse embryonic stem cells

2012-11-22 | GSE34170 | GEO

Super-enhancer driven LIF/LIFR-STAT3-SOX2 regulatory feedback loop promotes cancer stemness in head and neck squamous cell carcinoma (ATAC-seq)

Project description:Super-enhancers (SEs) have been recognized as key epigenetic regulators underlying cancer stemness and malignant traits by aberrant transcriptional control and promising therapeutic targets against human cancers. However, the SE landscape and their roles during head and neck squamous cell carcinoma (HNSCC) development especially in cancer stem cells (CSCs) maintenance remain underexplored yet. Here, we identified leukemia inhibitory factor (LIF)-SE as a representative oncogenic SE to activate LIF transcription in HNSCC. LIF secreted from cancer cells and cancer-associated fibroblasts promotes cancer stemness by driving SOX2 transcription in an autocrine or paracrine manner, respectively. Mechanistically, enhancer elements E1, 2, 4 within LIF-SE recruited SOX2/SMAD3/BRD4/EP300 to facilitate LIF transcription; LIF activated downstream LIFR-STAT3 signaling to drive SOX2 transcription, thus forming a previously unknown regulatory feedback loop (LIF-SE-LIF/LIFR-STAT3-SOX2) to maintain LIF overexpression and CSCs stemness. Clinically, increased LIF abundance in clinical samples correlated with malignant clinicopathological features and patient prognosis; higher LIF concentrations in presurgical plasma were negatively associated with patient survival and dramatically diminished following cancer eradication. Therapeutically, pharmacological targeting LIF-SE-LIF/LIFR-STAT3 significantly impaired tumor growth and reduced CSC subpopulations in HNSCC xenograft and PDX models. Our findings reveal a hitherto uncharacterized LIF-SE-mediated auto-regulatory loop in regulating HNSCC stemness and highlight LIF as a novel non-invasive biomarker and potential therapeutic target for HNSCC.

2024-11-06 | GSE274994 | GEO

Super-enhancer driven LIF/LIFR-STAT3-SOX2 regulatory feedback loop promotes cancer stemness in head and neck squamous cell carcinoma (ChIP-seq)

2024-11-06 | GSE274995 | GEO

Dual knockdown of Esrrb and Sox2 in mouse embryonic stem cells

Project description:Esrrb, Sox2 or Esrrb and Sox2 were knocked down in mouse ES cells using shRNA plasmid pSUPER.puro containing shRNAs from the publications Feng et al., 2009 and Rodda et al., 2005. Knockdown was transfected into mouse ES cells using lipofectamine and then cells were selected for knockdown using puromycin. RNA was harvested after 2 days of knockdown. Esrrb and Sox2 were knocked down in mouse ES cells either individually or together, cells were selected with puromycin and RNA harvested and subjected to microarray after 2 days.

2012-11-22 | E-GEOD-34170 | biostudies-arrayexpress

Identification the Expression of Sox2 in Colorectal Cancer Tissues

Project description:Sox2 has been studied in several types of human solid tumors. The investigators found that Sox2 had higher expression level in colorectal cancer and metastatic tissues than normal tissues. So the investigators assumed that whether Sox2 plays an important role in the progression and migration of colon cancer.

| 2124687 | ecrin-mdr-crc

ysblcc sox2

Project description:ysblcc sox2

| PRJEB2061 | ENA

MUC1-C PROMOTES CHRONIC INFLAMMATION IN THE PROGRESSION OF HEAD AND NECK SQUAMOUS CELL CARCINOMAS

Project description:Mucin 1 (MUC1) is aberrantly expressed in adenocarcinomas of epithelial barrier tissues and contributes to their progression. Less is known about involvement of MUC1 in the pathogenesis of squamous cell carcinomas (SCCs). The present work demonstrates that the MUC1 gene is upregulated in advanced head and neck SCCs (HNSCCs) and, as determined by scRNA-seq analysis, is expressed in the malignant cell populations of HNSCC tumors. Studies of HNSCC cell lines demonstrate that the MUC1-C subunit regulates expression of (i) RIG-I and MDA5 pattern recognition receptors, (ii) STAT1 and interferon (IFN) regulatory factors, and (iii) downstream IFN-stimulated genes (ISGs). MUC1-C integrates STAT1 with induction of the ∆Np63 and SOX2 genes that are aberrantly expressed in HNSCCs. We also show that MUC1-C/STAT1 signaling activates the NFE2L2 gene and, in turn, MUC1-C binds directly to NRF2 in regulating redox balance. In extending these HNSCC cell dependencies, we demonstrate that MUC1-C is necessary for NOTCH3 expression, self-renewal capacity and tumorigenicity. These results indicate that MUC1-C is a common effector that integrates STAT1-mediated chronic inflammation with regulation of the ∆Np63, SOX2, NRF2 and NOTCH3 TFs. Our findings indicate that MUC1-C drives progression of the HNSCC CSC state and is a target for advanced HNSCC treatment.

2024-04-23 | GSE252287 | GEO

Loss of SOX2 expression induces cell motility via vimentin up-regulation and is an unfavorable risk factor for survival of head and neck squamous cell carcinoma.

Project description:Recurrent gain on chromosome 3q26 encompassing the gene locus for the transcription factor SOX2 is a frequent event in human squamous cell carcinoma, including head and neck squamous cell carcinoma (HNSCC). Numerous studies demonstrated that SOX2 expression and function is related to distinct aspects of tumor cell pathophysiology. However, the underlying molecular mechanisms are not well understood, and the correlation between SOX2 expression and clinical outcome revealed conflicting data. Transcriptional profiling after silencing of SOX2 expression in a HNSCC cell line identified a set of up-regulated genes related to cell motility (e.g. VIM, FN1, CDH2). The inverse regulation of SOX2 and aforementioned genes was validated in 18 independent HNSCC cell lines from different anatomical sites. The inhibition of cell migration and invasion by SOX2 was confirmed by constant or conditional gene silencing and accelerated motility of HNSCC cells after SOX2 silencing was partially reverted by down-regulation of vimentin. In a retrospective study, SOX2 expression was determined by immunohistochemical staining on tissue microarrays containing primary tumor specimens of two independent HNSCC patient cohorts. Low SOX2 expression was found in 19.3% and 44.9% of primary tumor specimens, respectively. Univariate analysis demonstrated a statistically significant correlation between low SOX2 protein levels and reduced progression-free survival (Cohort I 51 vs. 16 months; Cohort II 33 vs. 12 months) and overall survival (Cohort I 150 vs. 37 months; Cohort II 33 vs. 16 months). Multivariate Cox proportional hazard model analysis confirmed that low SOX2 expression serves as an independent prognostic marker for HNSCC patients. We conclude that SOX2 inhibits tumor cell motility in HNSCC cells and that low SOX2 expression serves as a prognosticator to identify HNSCC patients at high risk for treatment failure.

| S-EPMC5528792 | biostudies-literature

Competitive binding of E3 ligases TRIM26 and WWP2 controls SOX2 in glioblastoma

Project description:The pluripotency transcription factor SOX2 is essential for the maintenance of glioblastoma stem cells (GSC), which drive tumor growth and treatment resistance.To understand how SOX2 is regulated in GSCs, we utilized a proteomic approach and identified the E3 ubiquitin ligase TRIM26 as a direct SOX2-interacting protein. Unexpectedly, we found TRIM26 depletion decreased SOX2 protein levels and increased SOX2 polyubiquitination in patient-derived GSCs, suggesting TRIM26 promotes SOX2 protein stability. Accordingly, TRIM26 knockdown reduced SOX2 transcriptional activity, self-renewal capacity, and in vivo tumorigenicity in multiple GSC lines. Mechanistically, we found TRIM26, via its C-terminal PRYSPRY domain, but independent of its RING domain, stabilizes SOX2 protein by directly inhibiting the interaction of SOX2 with WWP2, which we identify as a bona fide SOX2 E3 ligase in GSCs. Our work identifies E3 ligase competition as a critical mechanism of SOX2 regulation, with functional consequences for GSC identity and maintenance.

2021-11-04 | PXD028933 | Pride

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