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Transcriptome analysis of wildtype and rb1-/- zebrafish larval head tissue by RNA-Seq

ABSTRACT: The wild type and rb1 mutant transcriptomes were used to identify molecular pathways and epigenetic regulators altered in rb1 mutant brain cells. The data was also used for comparative analysis with zebrafish rb1-embryonal brain tumor transcriptome, to identify molecular pathways that distinguish transformed rb1- tumor cells from non-transformed rb1-/- mutant cells.

ORGANISM(S): Danio rerio

PROVIDER: GSE115720 | GEO | 2018/06/13

REPOSITORIES: GEO

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Transcriptome analysis of zebrafish wildtype adult brain and rb1-embryonal brain tumors by RNA-Seq

Project description:Zebrafish wildtype adult brain and rb1-embryonal brain tumor transcriptomes were used to identify candidate rb1-interacting chromatin remodelers and epigenetic regulators altered in rb1- transformed brain tumor cells. The data was also used for comparative analysis with zebrafish rb1-/- mutant transcriptome, to identify molecular pathways that distinguish transformed rb1- tumor cells from non-transformed rb1-/- mutant cells.

2018-06-13 | GSE115719 | GEO

Transcriptome analysis of zebrafish wildtype adult brain and rb1-embryonal brain tumors, and wildtype and rb1-/- zebrafish larval head tissue, by RNA-Seq

Project description:Transcriptome analysis of zebrafish wildtype adult brain and rb1-embryonal brain tumors, and wildtype and rb1-/- zebrafish larval head tissue, by RNA-Seq

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Murine Prostate Tissue: Rb1 null vs. Rb1 E2F binding deficient mutant

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Transcriptome analysis of zebrafish wildtype adult brain and rb1-embryonal brain tumors by RNA-Seq

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Delineating the Rb1 interactome data and its modulations during cell cycle progression.

Project description:The retinoblastoma (Rb) protein is a potent tumor suppressor which is known to negatively regulate the cell cycle as well as tumor progression. Phosphorylated Rb protein (pRb) has been demonstrated to be in-charge for the key G1 checkpoint, blocking entry into S-phase and thereby the cell growth. This study was designed to capture interacting protein partners of Rb1 as the cell cycle progresses. Rb1 expressing HEK-293 cells were cultured in light, medium and heavy SILAC labels to capture the changes in Rb1 interactome as the cell cycle progressed from G0 to G1S and then to G2 phase, respectively. This data might help in understanding the cell cycle regulatory effect of Rb1 protein and complement the available information on its interacting partners.

2017-09-14 | PXD007708 | Pride

The spliceosome is an exploitable vulnerability in RB1-mutant cancer

Project description:RB transcriptional corepressor 1 (RB1) is frequently mutated in human cancers, we discover a new target of oncogenic stress in RB1-mutant cells.

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Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

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Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Retinae from Rb1/p107 DKO and Rb1/p107/Hells TKO mice at postnatal day 21 were analyzed for gene expression using RNA-seq.

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RB1 expression and targeting by CDK4/6 inhibitors in small cell lung cancer

Project description:The canonical model of small cell lung cancer (SCLC) depicts tumors arising from dual inactivation of TP53 and RB1. However, many genomic studies have persistently identified tumors with no RB1 mutations. Here, we examined RB1 protein expression and function in SCLC. RB1 expression was examined by immunohistochemical analysis of 62 human SCLC tumors. These studies showed that ~14% of SCLC tumors expressed abundant RB1 protein, which is associated with neuroendocrine (NE) gene expression and is enriched in YAP1 expression, but no other lineage proteins that stratify SCLC. SCLC cells and xenograft tumors with RB1 protein expression were sensitive to growth inhibition by the CDK4/6 inhibitor palbociclib, and this inhibition was shown to be dependent on RB1 expression by CRISPR knockout. Furthermore, a patient with biopsy-validated wt RB1 SCLC who received the CDK4/6 inhibitor abemaciclib demonstrated a dramatic decrease in mutant TP53 ctDNA allelic fraction from 62.1% to 0.4% and decreased tumor mass on CT scans. Importantly, immunohistochemistry of the diagnostic biopsy specimen showed RB1 positivity. Finally, we identified a transcriptomics-based RB1 loss-of-function signature that discriminates between SCLC cells with or without RB1 protein expression and validated it in the patient who was responsive to abemaciclib, suggesting its potential use to predict CDK4/6 inhibitor response in SCLC patients. Our study demonstrates that RB1 protein is an actionable target in a subgroup of SCLC, a cancer that exhibits no currently targetable mutations.

2022-11-14 | GSE217646 | GEO

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