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Transcriptom analysis of MCF10A before and after H-RAS transformation [RNA-seq]

ABSTRACT: Transcriptom analysis of MCF10A before and after H-RAS transformation [RNA-seq]

PROVIDER: PRJNA589052 | ENA |

REPOSITORIES: ENA

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Regulatory regions of MCF10A before and after H-RAS transformation [ATAC-seq]

Project description:Regulatory regions of MCF10A before and after H-RAS transformation [ATAC-seq]

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Transcriptom analysis of MCF10A before and after H-RAS transformation [RNA-seq]

Project description:Gene transcription is substantially regulated by distant regulatory elements via combinatorial binding of transcription factors. It is more and more recognized that alterations in chromatin state and transcription factor binding in these distant regulatory elements may have key roles in cancer development. Here we focused on the first stages of oncogene induced carcinogenic transformation, and characterized the regulatory network underlying transcriptional reprogramming associated with this process. Using Hi-C data, we couple between differentially expressed genes and their differentially active regulatory elements and reveal two candidate transcription factors, p53 and CTCF, as major determinants of transcriptional reprogramming at early stages of HRas-induced transformation. Strikingly, the malignant transcriptional reprograming is promoted by redistribution of chromatin binding of these factors without major variation in their expression level. Our results demonstrate that alterations in the regulatory landscape have a major role in driving oncogene-induced transcriptional reprogramming.

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ChIP seq of CTCF and p53 in MCF10A before and after H-RAS transformation [ChIP-seq]

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Ribosome profiling and RNA sequencing of MCF10A-ER-Src and fibroblast cell transformation

Project description:We applied ribosome profiling and RNA sequencing to examine gene expression regulation during oncogenic cell transformation. One model involves normal mammary epithelial cells (MCF10A) containing ER-Src. Treatment of such cells with tamoxifen rapidly induces Src, thereby making it possible to kinetically follow the transition between normal and transformed cells. The other model consists of three isogenic cell lines derived from primary fibroblasts in a serial manner (Hahn et al., 1999). EH cell is immortalized by overexpression of telomerase (hTERT), and exhibits normal fibroblast morphology. EL cell expresses hTERT along with both large and small T antigens of Simian virus 40, and it displays an altered morphology but is not transformed. ELR cell expresses hTERT, T antigens, and an oncogenic derivative of Ras (H-RasV12).

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RAS-induced transformation of mammary epithelial cells relies on ZEB1-dependent cellular reprogramming through a paracrine process

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