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SMARCB1 Loss in Poorly-differentiated Chordomas Drives Tumor Progression

ABSTRACT: SMARCB1 Loss in Poorly-differentiated Chordomas Drives Tumor Progression

PROVIDER: PRJNA901898 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22298251_1.fastq.gz	Fastqsanger.gz
	SRR22298251_2.fastq.gz	Fastqsanger.gz
	SRR22298252_1.fastq.gz	Fastqsanger.gz
	SRR22298252_2.fastq.gz	Fastqsanger.gz
	SRR22298253_1.fastq.gz	Fastqsanger.gz

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SMARCB1 Loss in Poorly-differentiated Chordomas Drives Tumor Progression

Project description:Poorly-differentiated (PD) chordoma, a tumor found mainly in children, adolescents and young adults is a rare, aggressive tumor originating from notochordal tissue, with limited therapeutic options. SMARCB1, a core component of the BAF and PBAF chromatin remodeling complexes, is the most frequently mutated gene in PD chordomas, the most aggressive form of this cancer. In this study, we employed cellular models of SMARCB1-negative PD chordomas to characterize expression of SWI/SNF complex members and determine the impact of SMARCB1 re-expression on cell growth as well as the transcriptional landscape by RNA-seq. We generated 2 SMARCB1-negative PD chordoma cell lines, CH22 and UM-Chor5, with an inducible SMARCB1 expression system. After 72 hours of induction of SMARCB1 re-expression, we observed continued growth of both SMARCB1-negative PD chordoma cell lines. This is in striking contrast to SMARCB1-deficient rhabdoid cell lines, where we found SMARCB1 re-expression inhibits growth completely. We also found the lack of growth inhibition may arise from the loss of CDKN2A/p16INK4A expression in all poorly differentiated chordoma cell lines which correlated well with the gene expression data. SMARCB1 re-expression in both CH22 and UM-Chor5 cells showed downregulation for rRNA and RNA processing as well as metabolic processing. Upregulated differentially expressed genes included those involved in cell adhesion, cell migration, and development. Taken together, our data establish SMARCB1 re-expression in PD chordomas alters the repertoire of SWI/SNF complexes, perhaps restoring those associated with cellular differentiation. Our findings support a model where SMARCB1 inactivation blocks the conversion of growth-promoting SWI/SNF complexes to differentiation-inducing ones.

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SMARCB1 Loss in Poorly Differentiated Chordomas Drives Tumor Progression.

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Project description:Poorly differentiated thyroid carcinomas (PDTC) represent a heterogeneous, aggressive entity, presenting features that suggest a progression from well-differentiated carcinomas. To elucidate the mechanisms underlying such progression and identify novel therapeutical targets, we assessed the genome-wide expression in normal thyroid tissues, well-differentiated thyroid carcinomas and PDTC. RNA were extracted from 2 normal thyroid tissues taken from the opposite lobe of thyroid tumors, and 24 thyroid carcinomas: 5 PDTC, 7 classic papillary thyroid carcinomas (cPTC), 8 follicular variants of PTC (fvPTC) and 4 follicular thyroid carcinomas (FTC). All samples were obtained at time of surgery and immediately frozen in liquid nitrogen. We also hybridized a commercial pool of human thyroid total RNA (BD Bioscience). PTC were screened for BRAF mutations and rearrangements of RET/PTC and, in addition, follicular variants were also analyzed for RAS mutations and PAX8-PPARG rearrangements. FTC were screened for RAS and PAX8-PPARG rearrangements. PDTC were analyzed for BRAF, RAS and PAX8-PPARG genes.

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Project description:SMARCB1 (Snf5/Ini1/Baf47) is a potent tumor suppressor, the loss of which serves as the diagnostic feature in Malignant Rhabdoid Tumors (MRT) and Atypical Teratoid/Rhabdoid Tumors (AT/RT), two highly aggressive forms of pediatric neoplasms. Here, we restore Smarcb1 expression in cells derived from Smarcb1-deficient tumors which developed in Smarcb1-heterozygous p53-/- mice. Profiling Smarcb1 dependent gene expression we find genes which are dependent on Smarcb1 expression to be enriched for ECM and cell adhesion functions. We identify Igfbp7, which is related to the insulin-like growth factor binding proteins family, as a downstream target of Smarcb1 transcriptional activity, and show that re-introduction of Igfbp7 alone can hinder tumor development. Two cancer cell lines, 167 and 365, derived from Smarcb1-deficient tumors which developed in Smarcb1-heterozygous p53-/- mice were re-infected with a retro-viral vector for Smarcb1 re-expression or an empty retro-viral vector as control. Total-RNA was collected 3 days post infection so as to enrich for direct targets of Smarcb1 transcriptionaly regulated genes

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