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RAVER1 interconnects TGFB signaling, EMT and miR/RISC activity by modulating alternative splicing [A549_RAVER1_KD]

ABSTRACT: The depletion and deletion of RAVER1 substantially impairs the 2D-proliferation of tumor cells, vitality in 3D cell models and the growth of subcutaneous xenografts in nude mice. Disturbance of RAVER1 affects various cancer hallmark pathways manifesting in deregulated E2F/DREAM-controlled transcription and broadly hampered microRNA-dependent gene silencing. In carcinoma-derived cell models, impaired control by microRNAs (miR) leads to the upregulation of various tumor suppressors like BTG2, which is suppressed by the most abundant oncomiR 21-5p.

ORGANISM(S): Homo sapiens

PROVIDER: GSE232714 | GEO | 2023/06/14

REPOSITORIES: GEO

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RAVER1 interconnects lethal EMT and miR/RISC activity by the control of alternative splicing

Project description:The RAVER1 protein was proposed to serve as a co-factor in guiding the PTBP-dependent control of alternative splicing (AS). Whether RAVER1 solely acts in concert with PTBPs and how it affects cancer cell fate remained elusive. Here we provide the first comprehensive investigation of RAVER1-controlled AS in cancer cell models and reveal a pro-oncogenic role of RAVER1 in tumor growth. This unravels that RAVER1 guides AS in synergy with PTBPs but more prominently serves PTBP1-independent roles in splicing. In cancer cells, one major function of RAVER1 is the control of proliferation and apoptosis, which involves the modulation of AS events within the miR/RISC pathway. Associated with this regulatory role, RAVER1 antagonizes lethal, TGFB-driven epithelial-mesenchymal-transition (EMT) by limiting TGFB signaling. RAVER1-modulated splicing events affect the insertion of protein interaction modules in factors guiding miR/RISC-dependent gene silencing. Most prominently, in all three human TNRC6 proteins, RAVER1 controls AS of GW-enriched motifs, which are essential for AGO2-binding. Disturbance of RAVER1-guided AS events in TNRC6 proteins and other facilitators of miR/RISC activity compromise miR/RISC activity which is essential to restrict TGFB signaling and lethal EMT.

2024-01-11 | PXD043342 | Pride

Combinatorial analysis of miRNA and mRNA expression in pancreatic ductal adenocarcinoma (PDAC)_miRNA

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Synthetic circular miR-21 RNA decoys enhance tumor suppressor expression and impair tumor growth in mice (small RNA-Seq II)

Project description:Natural and synthetic circular RNAs effectively impair miRNA function. MiR-21-5p is a potent oncomiR presenting ~33% of all miRNAs across cancers, ~41% in lung adenocarcinoma (LUAD), and ~68% in LUAD-derived cells. We validate and identify five main tumor suppressors targeted by miR-21-5p by deletion of the MIR21 locus in LUAD cells. Synthetic, liposome-delivered circular miR-21-5p decoys enhance expression of these tumor suppressors and severely impair tumor cell vitality at low doses. Decoy efficacy is not increased by bulging of miR-21-5p targeting sites, but associated with substantial cellular decoy stability, indicated by a half-life of ~20h. The intraperitoneal application of nanoparticle-delivered miR-21-5p decoys significantly impairs tumor growth in mouse LUAD tumor models. Decoys are well tolerated and were enriched in lung tissue. However, despite low decoy abundance, tumor suppressor expression was only increased in subcutaneous tumors. These findings suggest nanoparticle-delivered circular miRNA decoys as potent therapeutics in cancer treatment.

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Synthetic circular miR-21 RNA decoys enhance tumor suppressor expression and impair tumor growth in mice (small RNA-Seq I)

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BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

Project description:The human BTG1 and BTG2 genes are targeted by genetic alterations in hematological malignancies. In this study we examined the unique and overlapping functions of Btg1 and Btg2 in mouse B cell development. Mice deficient for Btg1 and Btg2 displayed the strongest phenotype with a decrease in B cell numbers in bone marrow due to impaired B cell commitment and immature B cell differentiation. To determine the underlying mechanism, microarray expression analyis was performed on early (B220+ CD43+) and late (B220+ CD43-) B cells of WT and Btg1;Btg2 dKO mice. Total RNA obtained from sorted B220+ CD43+ ( Hardy fractions ABC) and B220+ CD43- (Hardy fractions DEF) BM cells of WT and Btg1-/-;Btg2-/- mice. In total 4 samples were analyzed and no replicates were included.

2014-03-19 | E-GEOD-55997 | biostudies-arrayexpress

BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

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