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Chip-chip from C-33 cells expressing FLAG-HPV1 E2 with FLAG-HPV1 E2

ABSTRACT: HPV1 E2 binds with Brd4 to host mitotic chromosomes. To identify the targets, chromatin was prepared from mitotic C-33 cells expressing HPV1 E2, and analyzed by ChIP-chip analysis for binding to a portion of the human genome. E2 and Brd4 bind to active promoters in interphase C-33 cells (Jang et al., 2009), however, in mitosis E2 was observed instead to bind to a few extremely broad peaks on several chromosomes. These peaks ranged in size from several hundred Kb to >1 Mb and, for the most part, overlapped coding regions. Signals of anti-FLAG E2 ChIP DNA from mitotic HPV1 E2 expressing C-33 cells

ORGANISM(S): Homo sapiens

SUBMITTER: Kui Shen

PROVIDER: E-GEOD-52312 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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mRNA expression in C-33A cells expressing HPV1 E2

Project description:Profile of RNA expression in a C-33A cell line derived from an HPV negative cervical carcinoma in the presence or absence of HPV1 E2 expression. mRNA profiles of C-33A cells in presence or absence of HPV1 E2 expression were generated by deep sequencing using Illumina GAIIx. Two samples (no replicates). One control and one experimental.

2014-04-14 | E-GEOD-52367 | biostudies-arrayexpress

SERBP1 iCLIP in mitotic and asynchronous cells with Blu577 treatment

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2021-10-05 | E-MTAB-10830 | biostudies-arrayexpress

Cdk1-mediated threonine phosphorylation of Sam68 modulates its RNA binding, alternative splicing activity, and cellular functions

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2023-03-11 | PXD032716 | Pride

Prediction and Testing of Novel Transcriptional Networks Regulating Embryonic Stem Cell Self-Renewal and Commitment

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2016-08-24 | E-GEOD-85968 | biostudies-arrayexpress

c-Src Modulates Estrogen-Induced Stress and Apoptosis in Estrogen-Deprived Breast Cancer Cells [MCF-7:5C]

Project description:The emergence of anti-estrogen resistance in breast cancer is an important clinical phenomenon affecting long-term survival in this disease. Identifying factors that convey cell survival in this setting may guide improvements in treatment. Estrogen (E2) can induce apoptosis in breast cancer cells that have been selected for survival after E2 deprivation for long periods (MCF-7:5C cells), but the mechanisms underlying E2-induced stress in this setting have not been elucidated. Here, we report that the c-Src kinase functions as a key adapter protein for the estrogen receptor (ER, ESR1) in its activation of stress responses induced by E2 in MCF-7:5C cells. E2 elevated phosphorylation of c-Src, which was blocked by 4-hydroxytamoxifen (4-OHT), suggesting that E2 activated c-Src through the ER. We found that E2 activated the sensors of the unfolded protein response (UPR), IRE1? (ERN1) and PERK kinase (EIF2AK3), the latter of which phosphorylates eukaryotic translation initiation factor-2? (eIF2?). E2 also dramatically increased reactive oxygen species production and upregulated expression of heme oxygenase HO-1 (HMOX1), an indicator of oxidative stress, along with the central energy sensor kinase AMPK (PRKAA2). Pharmacologic or RNA interference-mediated inhibition of c-Src abolished the phosphorylation of eIF2? and AMPK, blocked E2-induced ROS production, and inhibited E2-induced apoptosis. Together, our results establish that c-Src kinase mediates stresses generated by E2 in long-term E2-deprived cells that trigger apoptosis. This work offers a mechanistic rationale for a new approach in the treatment of endocrine-resistant breast cancer. MCF-7:5C cells were treated with vehicle (0.1% EtOH) as control, E2 (10-9mol/L), 4-OHT (10-6mol/L), E2 (10-9mol/L) plus 4-OHT (10-6mol/L), PP2 (5x10-6mol/L), and E2 (10-9mol/L) plus PP2 (5x10-6mol/L) respectively for 72 hours.

2014-07-18 | E-GEOD-59535 | biostudies-arrayexpress

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2015-12-07 | E-GEOD-72136 | biostudies-arrayexpress

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2010-12-21 | E-GEOD-24785 | biostudies-arrayexpress

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