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P21, ccng1, foxo3b and fbxw7 contribute to p53-dependent cell-cycle arrest [PNP IR]

ABSTRACT: p21, ccng1, foxo3b and fbxw7 contribute to p53-dependent cell-cycle arrest [PNP IR]

PROVIDER: PRJNA1218808 | ENA |

REPOSITORIES: ENA

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p21, ccng1, foxo3b and fbxw7 contribute to p53-dependent cell-cycle arrest [Mouse IR]

Project description:p21, ccng1, foxo3b and fbxw7 contribute to p53-dependent cell-cycle arrest [Mouse IR]

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p21, ccng1, foxo3b and fbxw7 contribute to p53-dependent cell-cycle arrest [MPNP timecross]

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p21, ccng1, foxo3b and fbxw7 contribute to p53-dependent cell-cycle arrest [MPNP 18hpf]

Project description:p21, ccng1, foxo3b and fbxw7 contribute to p53-dependent cell-cycle arrest [MPNP 18hpf]

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p21 Regulates LC Radiation Resistance

Project description:Treatment with ionizing irradiation (IR) may lead to accumulation of tumor-infiltrating T regulatory (Treg) cells and subsequent tumor resistance to radiotherapy. Here we focused on the contribution of Langerhans cells (LCs) to this phenomenon because of their unique ability to resist depletion by high-dose IR. We found that LCs resisted apoptosis and rapidly repaired DNA damage post-IR. Particularly, we found that p21 was overexpressed in LCs, and that p21-deficient LCs underwent apoptosis and accumulated DNA damage following IR treatment. Wild-type, but not p21-deficient, LCs upregulated major histocompatibility complex class II molecules, migrated to the draining lymph nodes and increased Treg cell numbers upon exposure to IR. These findings suggest a means for manipulating LC IR-resistance to increase cutaneous tumor response to radiotherapy. See above Cells were purified by flow cytometry and pooled until >10,000 cells/sample. At least 2 replicates of each sample were submitted.

2015-07-25 | E-GEOD-71330 | biostudies-arrayexpress

p21 Regulates LC Radiation Resistance

2015-07-25 | GSE71330 | GEO

FBXW7

Project description:FBXW7

| PRJNA783287 | ENA

FBXW7

Project description:Purpose: FBXW7 is one of the most frequently mutated tumor suppressors, the deficiency of which has been associated with resistance to some anticancer therapies. Through bioinformatic analyses and genome-wide CRISPR screens, we here reveal that FBXW7 deficiency leads to multi-drug resistance (MDR), to a bigger extent than well-established MDR-drivers such as ABCB1. Proteomic data from FBXW7-deficient cells and human cancer samples identify the upregulation of mitochondrial function as a hallmark of FBXW7 deficiency, which has been previously linked to an increased resistance to chemotherapy. Accordingly, genetic or chemical targeting of mitochondria is preferentially toxic for FBXW7-deficient cells. For instance, targeting mitochondrial translation with the antibiotic Tigecycline efficiently kills FBXW7-deficient cells in vitro and in vivo, by a mechanism that involves activation of the Integrated Stress Response (ISR). Searching for additional drugs that overcome MDR in FBXW7-deficient cells, we found several targeted therapies such as Erlotinib, Dasatinib or Vemurafenib which unexpectedly also activate the ISR. Together, our study reveals that one of the most frequent mutations in cancer reduces the sensitivity to the vast majority of available therapies, and identifies a general principle to overcome such resistance. Methods: This study was performed in 2 groups of DLD1 cells with duplicate samples per group. Both control (Wild Type, WT) and experimental (FBXW7 -/-, KO) were exposed to Tigecycline (10µM). DMSO was used as a control for the treatment. After 24h, the RNA was extracted and the transcriptome was profiled with RNA-Sequencing (RNA-seq) analysis. Results: our study reveals that one of the most frequent mutations in cancer reduces the sensitivity to the vast majority of available therapies, and identifies a general principle to overcome such resistance.

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Transcriptomic Analysis of pnp-1 mutants in C. elegans

Project description:We used RNA-seq to identify gene expression changes in C. elegans pnp-1 mutants

2021-04-14 | GSE165786 | GEO

Effect of FBXW7 loss and concomitant FBXW7-KMT2D loss on mRNA levels

Project description:We assessed the role of the E3 ligase FBXW7 in mature B-cell neoplasms. This experiment assesses the role of the FBXW7-KMT2D axis in regulating gene expression in OPM-1 cells.

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Pseudomonas sp. PNP

Project description:Pseudomonas sp. PNP Genome sequencing and assembly

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