Change expression of genes in iron chelation and deficient conditions
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ABSTRACT:
PROVIDER: PRJNA431603 | ENA |
REPOSITORIES: ENA
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Project description:Firstly, cell senescence and anti-oxidant genes were down-regulated by iron deficient mice and iron-specific chelator deferoxamine (DFO) using a DNA microarray. Our data suggested that down-regulation of anti-oxidant genes and cell senescence gene induced oxidative stress in iron-deficient and -specific chelated condition.
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Project description:Iron accumulation in cancer cells contributes to malignant progression and chemoresistance. While disrupting this process can influence various hallmarks of cancer, the immunomodulatory effects of chelating iron in tumors remain undefined. Here, we report that treatment with deferiprone, an FDA-approved iron chelator, elicits innate immune responses that control metastatic ovarian cancer. Deferiprone reprogrammed ovarian cancer cells towards an immunostimulatory state characterized by enhanced production of type I interferon (IFN) and surface overexpression of molecules that activate natural killer (NK) cells. Mechanistically, this reprogramming was driven by innate sensing of mitochondrial DNA in the cytosol and concomitant activation of nuclear DNA damage responses evoked upon iron chelation. Deferiprone administration synergized with chemotherapy and prolonged the survival of mice bearing metastatic ovarian cancer by bolstering intratumoral NK cell infiltration and type I IFN responses. Iron chelation may represent an alternative immunotherapeutic approach for malignancies that are normally refractory to T cell-centric modalities.
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Project description:Transcriptional profile of whole roots of wild-type and pye-1 mutants exposed to 24 hours -Fe were generated Global population increases and climate change underscore the need for better comprehension of how plants acquire and process nutrients such as iron. A systems biology approach was taken to elucidate novel regulatory mechanisms involved in plant responses to iron deficiency (-Fe). Using cell-type specific transcriptional profiling we identified a pericycle-specific iron deficiency response, and a previously uncharacterized transcription factor, POPEYE (PYE), that plays an important role in this response. Functional analysis of PYE suggests that it positively regulates growth and development under iron deficient conditions. ChIP-on-chip analysis and transcriptional profiling reveal that PYE helps maintain iron homeostasis by directly and indirectly regulating the expression of ferric reductases, metal ion transporters, iron storage proteins, and other key iron homeostasis genes. In addition to PYE, we also identified a second protein BRUTUS (BTS), which appears to negatively regulate the response to iron deficiency. BTS is a unique putative E3 ligase protein, with metal ion binding and DNA binding domains. PYE and BTS are tightly co-regulated and physically interact with PYE paralogs, one of which is thought to positively regulate expression of genes involved in iron homeostasis. We propose that iron content is sensed within the pericycle where PYE, perhaps in conjunction with BTS and other regulatory proteins, is then activated to control a regulatory network involved in maintaining proper iron distribution in plants. Keywords: Expression analysis To determine how loss of PYE expression affects the transcriptional profile of whole roots, pye-1 mutants and wild-type seeds were germinated under standard growth conditions then transferred to standard media (control, MS media) or iron deficient media (-Fe, 0.3mM Ferrozine in MS media containing no ferrous sulfate). After 24 hours of exposure to +Fe or -Fe whole roots were collected and analyzed.
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Dynamic model of iron distribution in mice. This model includes only normal iron with the parameters that fit the data from Lopes et al. 2010 for mice fed a deficient iron diet.
This model does not include the radioiron tracer species. It is appropriate to study the properties in conditions where no tracers are used (for example for steady state analysis).
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Project description:Transcriptional profile of whole roots of wild-type and pye-1 mutants exposed to 24 hours -Fe were generated Global population increases and climate change underscore the need for better comprehension of how plants acquire and process nutrients such as iron. A systems biology approach was taken to elucidate novel regulatory mechanisms involved in plant responses to iron deficiency (-Fe). Using cell-type specific transcriptional profiling we identified a pericycle-specific iron deficiency response, and a previously uncharacterized transcription factor, POPEYE (PYE), that plays an important role in this response. Functional analysis of PYE suggests that it positively regulates growth and development under iron deficient conditions. ChIP-on-chip analysis and transcriptional profiling reveal that PYE helps maintain iron homeostasis by directly and indirectly regulating the expression of ferric reductases, metal ion transporters, iron storage proteins, and other key iron homeostasis genes. In addition to PYE, we also identified a second protein BRUTUS (BTS), which appears to negatively regulate the response to iron deficiency. BTS is a unique putative E3 ligase protein, with metal ion binding and DNA binding domains. PYE and BTS are tightly co-regulated and physically interact with PYE paralogs, one of which is thought to positively regulate expression of genes involved in iron homeostasis. We propose that iron content is sensed within the pericycle where PYE, perhaps in conjunction with BTS and other regulatory proteins, is then activated to control a regulatory network involved in maintaining proper iron distribution in plants. Keywords: Expression analysis
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Project description:Iron chelation therapy elicits innate immune control of metastatic ovarian cancer
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