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Alternative splicing regulation of cell cycle genes by SPF45/SR140/CHERP complex controls cancer cell proliferation

ABSTRACT: Alternative splicing regulation of cell cycle genes by SPF45/SR140/CHERP complex controls cancer cell proliferation

PROVIDER: PRJNA749954 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15257928_1.fastq.gz	Fastqsanger.gz
	SRR15257928_2.fastq.gz	Fastqsanger.gz
	SRR15257929_1.fastq.gz	Fastqsanger.gz
	SRR15257929_2.fastq.gz	Fastqsanger.gz
	SRR15257930_1.fastq.gz	Fastqsanger.gz

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PPIB-regulated alternative splicing of cell cycle gene contributes to its regulation of cell proliferation

Project description:PPIB-regulated alternative splicing of cell cycle gene contributes to its regulation of cell proliferation

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Regulation of NUMB alternative splicing by RBM5, RBM6 and RBM10 controls cancer cell proliferation

Project description:RBM5, a regulator of alternative splicing of apoptotic genes, and its close homologues, RBM6 and RBM10, are RNA binding proteins frequently deleted or mutated in lung cancer. We report that RBM5/6 and RBM10 antagonistically regulate the proliferative capacity of cancer cells and display distinct positional effects in alternative splicing regulation. We identify the Notch pathway regulator NUMB as a key target of these factors in the control of cell proliferation. NUMB alternative splicing, which is frequently altered in lung cancer, can regulate colony and xenograft tumor formation and its modulation recapitulates or antagonizes the effects of RBM5, 6 and 10 in cell colony formation. RBM10 mutations identified in lung cancer cells disrupt NUMB splicing regulation to promote cell growth. Our results reveal a key genetic circuit in the control of cancer cell proliferation. RNA from 3 biological replicates of knockdowns of RBM5, 6 and 10 and a control set were used. Changes between the control and knockdowns were measured based on using a splice-junction array (Affymetrix HJAY).

2013-12-20 | E-GEOD-47431 | biostudies-arrayexpress

Regulation of NUMB alternative splicing by RBM5, RBM6 and RBM10 controls cancer cell proliferation (CLIP-Seq)

Project description:RBM5, a regulator of alternative splicing of apoptotic genes, and its close homologues, RBM6 and RBM10, are RNA binding proteins frequently deleted or mutated in lung cancer. We report that RBM5/6 and RBM10 antagonistically regulate the proliferative capacity of cancer cells and display distinct positional effects in alternative splicing regulation. We identify the Notch pathway regulator NUMB as a key target of these factors in the control of cell proliferation. NUMB alternative splicing, which is frequently altered in lung cancer, can regulate colony and xenograft tumor formation and its modulation recapitulates or antagonizes the effects of RBM5, 6 and 10 in cell colony formation. RBM10 mutations identified in lung cancer cells disrupt NUMB splicing regulation to promote cell growth. Our results reveal a key genetic circuit in the control of cancer cell proliferation. CLIP-Seq analysis of RBM5, RBM6 and RBM10, with 2 biological replicates and one non-specific control for each protein.

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An extensive program of periodic alternative splicing linked to cell cycle progression

Project description:Progression through the mitotic cell cycle requires periodic regulation of gene function at the levels of transcription, translation, protein-protein interactions, post-translational modification and degradation. However, the role of alternative splicing (AS) in the temporal control of cell cycle is not well understood. By sequencing the human transcriptome through two continuous cell cycles, we identify ~1,300 genes with cell cycle-dependent AS changes. These genes are significantly enriched in functions linked to cell cycle control, yet they do not significantly overlap genes subject to periodic changes in steady-state transcript levels. Many of the periodically spliced genes are controlled by the SR protein kinase CLK1, whose level undergoes cell cycle-dependent fluctuations via an auto-inhibitory circuit. Disruption of CLK1 causes pleiotropic cell cycle defects and loss of proliferation, whereas CLK1 over-expression is associated with various cancers. These results thus reveal a large program of CLK1-regulated periodic AS intimately associated with cell cycle control.

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Regulation of NUMB alternative splicing by RBM5, RBM6 and RBM10 controls cancer cell proliferation

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IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

Project description:IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

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IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

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PPIB-regulated alternative splicing of cell cycle gene contributes to its regulation of cell proliferation

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