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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shMORC2 mRNA-seq]

ABSTRACT: To investigate the role MORC2 plays in alternative splicing, we generated SW480 cell lines in which MORC2 was knocked down by shRNA.We then performed RNA-seq data for alternative splicing gene analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE246909 | GEO | 2024/08/02

REPOSITORIES: GEO

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [shRBM39 mRNA-seq]

Project description:To investigate the role RBM39 plays in alternative splicing, we generated SW480 cell lines in which RBM39 was knocked down by shRNA.We then performed RNA-seq data for alternative splicing gene analysis.

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [RBM39 RIP-seq]

Project description:RNA immunoprecipitation sequencing (RIP-seq) for the detection of RBM39 protein-binding RNA in SW480 cells.

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Global Regulation of Alternative RNA Splicing by the SR-Rich Protein RBM39

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MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

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Global Regulation of Alternative RNA Splicing by the SR-Rich Protein RBM39 CLIP-seq

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MORC2 promotes renal carcinogenesis via epigenetically downregulating DAPK1

Project description:epigenetic regulation plays a vital role in renal carcinogenesis. Here，we found epigenetic regulator MORC2 promoted carcinogenesis in kidney. Mechanistically, MORC2 functioned as oncogene via epigenetically silencing canonical tumor suppressor DAPK1 in kidney. Therefore, aMORC2—DAPK1 pro—oncogenic axis was identified in kindey.

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Co-regulation of alternative splicing by hnRNPM and ESRP1 during EMT

Project description:The epithelial-mesenchymal transition (EMT) is a fundamental developmental process that is abnormally activated in cancer metastasis. Dynamic changes in alternative splicing occur during EMT. ESRP1 and hnRNPM are splicing regulators that promote an epithelial splicing program and a mesenchymal splicing program, respectively. The functional relationships between these splicing factors in the genome-scale remain elusive. Comparing alternative splicing targets of hnRNPM and ESRP1 revealed that they co-regulate a set of cassette exon events, with the majority showing discordant splicing regulation. hnRNPM discordantly regulated splicing events show a positive correlation with splicing during EMT while concordant splicing events do not, highlighting the antagonistic role of hnRNPM and ESRP1 during EMT. Motif enrichment analysis near co-regulated exons identifies guanine-uridine rich motifs downstream of hnRNPM-repressed and ESRP1-enhanced exons, supporting a model of competitive binding to these cis-elements to antagonize alternative splicing. The set of co-regulated exons are enriched in genes associated with cell-migration and cytoskeletal reorganization, which are pathways associated with EMT. Splicing levels of co-regulated exons are associated with breast cancer patient survival and correlate with gene sets involved in EMT and breast cancer subtypes. In conclusion, hnRNPM and ESRP1 co-regulate antagonistically a set of alternative splicing events that occur during EMT. This regulation is likely mediated through competition for the same intronic binding sites downstream of variable exons. hnRNPM and ESRP1 regulated splicing events are associated with breast cancer survival.

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An EMT-driven alternative splicing program occurs in human breast cancer and modulates cellular phenotype.

Project description:Regulation of cell-cell junction formation and regulation of cell migration were enriched among EMT (Epithelial-Mesenchymal Transition)-associated alternatively splicing events. Our analysis suggested that most EMT-associated alternative splicing events are regulated by one or more members of the RBFOX, MBNL, CELF, hnRNP or ESRP classes of splicing factors. The EMT alternative splicing signature was confirmed in human breast cancer cell lines, which could be classified into basal and luminal subtypes based exclusively on their EMTassociated splicing pattern. Expression of EMT-associated alternative mRNA transcripts was also observed in primary breast cancer samples, indicating that EMT-dependent splicing changes occur commonly in human tumors. The functional significance of EMT-associated alternative splicing was tested by expression of the epithelial-specific splicing factor ESRP1 or depletion of RBFOX2 in mesenchymal cells, both of which elicited significant changes in cell morphology and motility towards an epithelial phenotype, suggesting that splicing regulation alone can drive critical aspects of EMT-associated phenotypic changes. The molecular description obtained here may aid in the development of new diagnostic and prognostic markers for analysis of breast cancer progression. Examination of transcriptomes of HMLE/Twist-ER before and after induction of EMT by tamoxifen

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