Identification of PRMT5-dependent genes in ESA+CD24lowCD44+ MCF7 cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE107762 | GEO | 2017/12/31
SECONDARY ACCESSION(S): PRJNA421322
REPOSITORIES: GEO
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Project description:Identification of PRMT5-dependent genes in ESA+CD24lowCD44+ MCF7 cells
| PRJNA421322 | ENA
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Project description:We identified distinct sets of genes under the control of PRMT5 and E2F1. Some of the most highly regulated genes, such as cortactin/CTTN, influenced cell migration, invasion and adherence. We characterised the functional role of the cortactin/CTTN gene, which enabled PRMT5 through E2F1 to promote cellular migration and invasion, whilst decreasing cellular adherence. Most significantly, there was a striking coincidence between the expression of PRMT5 and E2F1 in certain human tumours, and elevated levels of PRMT5, E2F1 and cortactin/CTTN correlated with poor prognosis disease. Our results suggest a causal relationship between PRMT5, E2F1 and the migration and invasion of cancer cells, thereby highlighting an important pathway that contributes to the cancer biology of tumour cells.
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Project description:Long non-coding Rnas (lncRNAs) can act as oncogenes or tumor suppressors to regulate cancer development. We found that CYP1B1-AS1 was down-regulated in breast cancer tissues and correlated with the prognosis of patients. Lentiviral vectors were used to overexpress CYP1B1-AS1 in MCF7 cells, and the target proteins bound to CYP1B1-AS1 were detected by pulldown assay and mass spectrometry. The function of CYP1B1-AS1 is unknown. Our study revealed the molecular mechanism of CYP1B1-AS1 inhibiting breast cancer proliferation in breast cancer, and provided a new strategy for the treatment of breast cancer targeting lncRNA.
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Project description:It has been reported that PHF1, CUL4B and PRMT5 all play important roles in epigenetic regulation. We reported that PHF1, CRL4B and PRMT5 may act as a complex in transcriptional regulation and have a vital effect in breast cancer progression. So we performed ChIP-on-chip assays to find unique promoters co-targeted by PHF1, CUL4B and PRMT5. PHF1, CUL4B and PRMT5 have a predominant cooperation, at least in MDA-MB-231 cells. comparison of PHF1, CUL4B and PRMT5 target genes
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Project description:Comprehensive RNA-seq experiments in DMSO and HPTB (inhibitor of PRMT5) treated cells delineate the role of PRMT5 complex in promoting breast cancer oncogenesis
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Project description:Comprehensive RNA-seq experiments in control and PRMT5 and WDR77 shRNA infected cells delineate the role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis
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Project description:Neuroblastoma (NB) is a devastating childhood cancer that remains clinically unmet. There is an urgency to develop new approaches to treat the disease. Protein arginine methyltransferase (PRMT5) is over-expressed in a wide variety of cancers and has been implicated with a key oncogenic role, achieved in part through its control of the master transcription regulator E2F1. Here, we have investigated the relevance of the interplay between PRMT5 and E2F1 in neuroblastoma and found that elevated expression occurs in poor prognosis high-risk disease. Cell lines derived from NB that recapitulate high PRMT5 and E2F1 expression exhibit increased levels of alternative RNA splicing compared to their low expression cell counterparts. Cancer-relevant exon-skipping events in apoptotic genes were apparent in high expressing NB cells which resulted in protein isoforms with decreased apoptotic activity. Pharmacological inhibition of PRMT5 or inactivation of E2F1 activity reduced exon skipping and reinstated normal apoptotic activity. Our findings show that a cancer relevant alternative splicing programme desensitises high risk NB to apoptosis. The critical role ascribed to PRMT5 and E2F1 in attaining the alterative RNA splicing programme equally identifies PRMT5 as a potential therapeutic target for neuroblastoma disease.
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Project description:Although an important association between lymph node metastasis and poor prognosis in breast cancer was observed decades ago, an active role for the lymphatic system in metastatic dissemination has only recently been examined. We demonstrate that the Six1 homeoprotein promotes peri- and intra-tumoral lymphangiogenesis, lymphatic invasion, and distant metastasis of breast cancer cells. We identify the pro-lymphangiogenic factor, VEGF-C, as required for this process, and demonstrate transcriptional induction as the mechanism of regulation of VEGF-C expression by Six1. Using a different, but complementary animal model, we show that while required, VEGF-C is not sufficient for the pro-metastatic effects of Six1. Verifying the clinical significance of this pro-metastatic Six1-VEGF-C axis, we demonstrate co-expression of Six1 and VEGF-C in human breast cancer. Two Control and two Six1 expressing MCF7 clones were orthotopically injected into NOD/Scid mice forming a total of 3 Control and 3 Six1 tumors that were allowed to grow to 2 cm^3 . The tumors were dissected and total RNA was isolated from each tumor and hybridized to Affymetrix arrays
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