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Transcriptional profilng of CCNE1 overexpressing hTERT-immortalized p53-R175H fallopian tube cell lines (FT282)

ABSTRACT: In this study we used RNA-seq to profile transcriptional changes in two clones of FT282-hTERT p53-R175H cells engineered to overexpress CCNE1. We compared the differential gene expression (DGE) of CCNE1 OE to their wild type counterparts and identified that CCNE1 OE increases expression of genes involved in G2/M progression. Subsequent gene set enrichment analysis (GSEA) revealed significant enrichment of genes co-regulated by MYBL2 and FOXM1 transcription factors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171453 | GEO | 2022/02/15

REPOSITORIES: GEO

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Transcriptional profilng of CCNE1 overexpressing hTERT-immortalized p53-R175H fallopian tube cell lines (FT282)

Project description:Transcriptional profilng of CCNE1 overexpressing hTERT-immortalized p53-R175H fallopian tube cell lines (FT282)

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Global binding profiles of MYBL2 and FOXM1 in lung adenocarcinoma reveal that MYBL2 regulates FOXM1 to control cell-cycle genes including CENPA [ChIP-seq]

Project description:MYBL2 is a transcription factor that has either pro-survival or anti-survival functions in a cell-type specific manner. Overexpression of MYBL2 is associated with worse survival of lung adenocarcinoma, but the mechanism by which it regulates transcription has not yet been elucidated. In this study, we found that MYBL2 mainly binds to the promoters of highly expressed genes in lung adenocarcinoma cells using ChIP-seq. Using knock-down and RNA-seq approach, we identified over a thousand of genes deregulated by MYBL2. By integrating ChIP-seq and RNA-seq data, we identified target genes of MYBL2. We revealed that FOXM1 is regulated by MYBL2 in lung adenocarcinoma cells, and FOXM1 binding sites are largely shared with MYBL2 binding sites. We treated lung adenocarcinoma cells with FDI-6, a known FOXM1 inhibitor and investigated the effect of FDI-6 in transcriptional regulation of MYBL2 and FOXM1. We found that CENPA is one of the key genes regulated by MYBL2 and FOXM1, and that it can be inhibited by FDI-6. Our signaling pathway analysis results revealed that MYBL2 and FOXM1 activate cell-cycle genes, suggesting that MYBL2 and FOXM1 act as oncogenic transcription factors in lung adenocarcinoma cells and FDI-6 could be a potential treatment of the disease.

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Global binding profiles of MYBL2 and FOXM1 in lung adenocarcinoma reveal that MYBL2 regulates FOXM1 to control cell-cycle genes including CENPA [RNA-seq]

2022-11-02 | GSE201270 | GEO

CCNE1 interactome analysis in HEK293T cells under the treatment of different CCNE1(:CDK2) ligands

Project description:This is to explore potential functional effects of CCNE1(:CDK2) ligands and compare them side by side.

2024-09-03 | PXD048328 | Pride

Array CGH reveals genetic homogeneity and frequent copy number increases encompassing CCNE1 in Fallopian tube carcinoma

Project description:Fallopian tube carcinoma (FTC) is a rare, poorly studied and aggressive cancer, associated with poor survival. Since tumorigenesis is related to acquisition of genetic changes, we used genome-wide array CGH to analyze copy number aberrations occurring in FTC in order to obtain a better understanding of FTC carcinogenesis and to identify prognostic events and targets for therapy. We used arrays of 2464 genomic clones, providing ~1.4 Mb resolution across the genome to quantitatively map genomic DNA copy number aberrations from fourteen FTC onto the human genome sequence. All tumors showed a high frequency of copy number aberrations with recurrent gains on 3q, 6p, 7q, 8q, 12p, 17q, 19 and 20q, and losses involving chromosomes 4, 5q, 8p, 16q, 17p, 18q and X. Recurrent regions of amplification included 1p34, 8p11-q11, 8q24, 12p, 17p13, 17q12-q21, 19p13, 19q12-q13 and 19q13. Candidate, known oncogenes mapping to these amplicons included CMYC (8q24), CCNE1 (19q12-q21) and AKT2 (19q13), whereas PIK3CA and KRAS, previously suggested to be candidate driver genes for amplification mapped outside copy number maxima on 3q and 12p, respectively. The FTC were remarkably homogeneous, with some recurrent aberrations occurring in more than 70% of samples, which suggests a stereotyped pattern of tumor evolution. Keywords: array CGH, CCNE1, AKT2, Fallopian tube cancer

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Transcriptional adaptation to DNA replication stress induced by CCNE1 overexpression

Project description:We overproduced human cyclin E from a stably-integrated inducible CCNE1 transgene in RPE1-hTERT cells over a period of weeks. CCNE1 overproduction induced replication stress, then slow proliferation, followed by adaptation to normal growth phenotype. We analyzed mRNA transcripts at key points of the timecourse: control, 2 days, 15-18 days, 39-51 days, and at a point several weeks after induction was withdrawn

2021-10-01 | GSE171845 | GEO

A polymorphic intronic enhancer at 19q12 drives CCNE1 expression in bladder cancer cells

Project description:We performed chromatin immunoprecipitation against a marker of active regulatory elements in bladder cancer cell lines to highlight regulatory regions specific to the bladder cancer genome. We then compared our dataset to other publicly available datasets to identify any novel, bladder-specific regulatory regions that also overlap with bladder-associated inherited polymorphisms. We used this procedure to determine that there is an intronic enhancer within the CCNE1 gene that binds KLF5 and modulates CCNE1 expression.

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MYBL2 promotes proliferation and metastasis of bladder cancer through transactivation of CDCA3

Project description:The transcription factor MYB proto-oncogene like 2 (MYBL2) plays a critical role in the regulation of gene expression and tumorigenesis. However, the biological function of MYBL2 in bladder cancer (BLCA) remains to be elucidated. Here, we first revealed that MYBL2 was elevated in BLCA tissues and was significantly correlated with clinicopathological parameters and cancer-specific survival of BLCA patients. Phenotypic assays showed that MYBL2 deficiency suppressed the proliferation and migration of BLCA cells in vitro and in vivo, whereas overexpression of MYBL2 contributed to the opposite phenotype. Mechanistically, MYBL2 could bind to the promoter of its downstream target gene cell division cycle-associated protein 3 (CDCA3) and transactivate it, which in turn promoted the malignant phenotype of BLCA cells. Further investigations revealed that MYBL2 interacted with forkhead box M1 (FOXM1) to co-regulate the transcription of CDCA3. In addition, MYBL2 and CDCA3 may activate the Wnt/β-catenin signaling by inhibiting the suppressor dickkopf-1 (DKK1), thereby regulating the malignant phenotype of BLCA cells. In conclusion, the current study has identified MYBL2 as an oncogene in BLCA. MYBL2 can accelerate the proliferation and metastasis of BLCA through the transactivation of CDCA3.

2022-05-02 | GSE201875 | GEO

MYBL2 promotes proliferation and metastasis of bladder cancer through transactivation of CDCA3

2022-05-04 | GSE201979 | GEO

Gene expression of DREAM complex-related inducible knockouts in HeLa cells

Project description:The DREAM complex and interacting proteins (e.g., BMYB and FOXM1) together control cell cycle-dependent gene expression. We identified an unexpected, specific kinetochore defect phenotype after depletion of a DREAM complex member (LIN52) in optical pooled CRISPR knockout screens of essential genes. Here we generated individual doxycycline-inducible Cas9 cell lines expressing lentiviral-integrated sgRNAs targeting LIN52, MYBL2, and FOXM1 to evaluate differential roles in gene expression regulaion.

2021-11-22 | GSE188631 | GEO

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