ZNF750 is a lineage-specific tumor suppressor in squamous cell carcinoma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA339991 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4054618_1.fastq.gz | Fastqsanger.gz | |||
| SRR4054618_2.fastq.gz | Fastqsanger.gz | |||
| SRR4054619_1.fastq.gz | Fastqsanger.gz | |||
| SRR4054619_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:ZNF750 controls epithelial homeostasis by regulating epidermal-differentiation genes, a role underscored by its pathogenic mutations in esophageal squamous cell cancers (SCCs). However, the precise role of ZNF750 in SCC cell biology remains unclear. In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotype of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a LncRNA (TINCR) which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. Together, our findings characterize ZNF750 as a crucial SCC-specific suppressor and uncover its novel anticancer-associated functions. Gene expression profile in CaSki following ZNF750 overexpression was examined by microarray gene expression analysis. To explore genes regulated by ZNF750 in squamous cell carcinoma, total RNA was isolated in biologic duplicate from CaSki either with ectopic expression of GFP (as control) or ZNF750, and hybridized to Affymetrix HG-U133 2.0 Plus arrays.
2016-08-25 | E-GEOD-86013 | biostudies-arrayexpress
Project description:ZNF750 controls epithelial homeostasis by regulating epidermal-differentiation genes, a role underscored by its pathogenic mutations in esophageal squamous cell cancers (SCCs). However, the precise role of ZNF750 in SCC cell biology remains unclear. In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotype of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a LncRNA (TINCR) which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. Together, our findings characterize ZNF750 as a crucial SCC-specific suppressor and uncover its novel anticancer-associated functions. RNA expression profile in UMSCC1 following ZNF750 wildtype overexpressing was analyzed by RNA-Seq.
2016-08-25 | E-GEOD-86014 | biostudies-arrayexpress
Project description:ZNF750 controls epithelial homeostasis by regulating epidermal-differentiation genes, a role underscored by its pathogenic mutations in esophageal squamous cell cancers (SCCs). However, the precise role of ZNF750 in SCC cell biology remains unclear. In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotype of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a LncRNA (TINCR) which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. Together, our findings characterize ZNF750 as a crucial SCC-specific suppressor and uncover its novel anticancer-associated functions.
2016-08-25 | GSE86014 | GEO
Project description:ZNF750 controls epithelial homeostasis by regulating epidermal-differentiation genes, a role underscored by its pathogenic mutations in esophageal squamous cell cancers (SCCs). However, the precise role of ZNF750 in SCC cell biology remains unclear. In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotype of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a LncRNA (TINCR) which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. Together, our findings characterize ZNF750 as a crucial SCC-specific suppressor and uncover its novel anticancer-associated functions. Gene expression profile in CaSki following ZNF750 overexpression was examined by microarray gene expression analysis.
2016-08-25 | GSE86013 | GEO
Project description:ZNF750 is a lineage-specific tumor suppressor in squamous cell carcinoma [CaSki]
| PRJNA339995 | ENA
Project description:ZNF750 is a lineage-specific tumor suppressor in squamous cell carcinoma [UMSCC1]
| PRJNA339994 | ENA
Project description:Quantitative proteomic profiling the lung squamous carcinoma cells
2016-07-14 | MSV000079911 | MassIVE
Project description:Lung squamous cell carcinoma (LUSC) is associated with high mortality and limited targeted therapies. USP13 is one of the most amplified genes in LUSC, and yet its role in lung cancer is largely unknown. Here, we establish a novel mouse model of LUSC by overexpressing USP13 in KrasG12D/+; Trp53flox/flox background (KPU). KPU model faithfully recapitulates the key pathohistological, molecular features, and cellular pathways of human LUSC. We found that USP13 altered lineage-determining factors such as NKX2-1 and SOX2 in club cells (CC10+) of the airway and reinforced the fate of club cells to squamous carcinoma development. We also showed a strong molecular association between USP13 and MYC, leading to the upregulation of squamous programs in murine and human lung cancer cells. Collectively, our data demonstrate USP13 as a molecular driver of lineage plasticity in club cells and provide mechanistic insight that may have potential implications for the treatment of NSCLC.
2024-01-02 | GSE244847 | GEO
Project description:ZNF750 controls epithelial homeostasis by regulating epidermal-differentiation genes, a role underscored by its pathogenic mutations in esophageal squamous cell cancers (SCCs). However, the precise role of ZNF750 in SCC cell biology remains unclear. In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotypes of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a long non-coding RNA (TINCR), which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. Together, our findings characterize ZNF750 as a crucial SCC-specific suppressor and uncover its novel anticancer-associated functions.
| S-EPMC5415641 | biostudies-literature
Project description:SMAD4 is a tumor suppressor mutated or silenced in multiple cancers including oral squamous cell carcinoma (OSCC). Human clinical samples and cell lines, mouse models and organoid culture were used to investigate the role that SMAD4 plays in progression from benign disease to invasive OSCC. Human OSCC lost detectable SMAD4 protein within tumor epithelium in 24% of cases and this loss correlated with worse progression free survival independent of other major clinical and pathological features. In a mouse model, Kras mutation induced benign papillomas while additional loss of Smad4 expression resulted in rapid development of invasive carcinoma. Examining regulatory pathways in organoids from SMAD4+ and SMAD4- mouse tumors, we found that either loss of SMAD4 or inhibition of TGFb signaling upregulated the WNT pathway and altered the extracellular matrix. The gene signature of the mouse tumor organoids lacking SMAD4 was highly similar to the gene signature of human head and neck squamous cell carcinoma. In summary, this work has uncovered novel mechanisms by which SMAD4 acts as a tumor suppressor in OSCC.
2024-05-14 | GSE228584 | GEO