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Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation [Cut&Tag]

ABSTRACT: Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation [Cut&Tag]

PROVIDER: PRJNA1129876 | ENA |

REPOSITORIES: ENA

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Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation [Cut&Tag]

Project description:It is well-known that p53-mediated gene regulation exerts a profound impact on the occurrence, progression, metastasis, and various other facets of tumor. Wherein, activation of p53 downstream DNA damage repair-related genes is able to promote the survival of cancer cells during tumor progression.Notably, it has been substantiated that the transcriptional activity of p53 could be modulated by interactions with other proteins.Therefore, we asked whether the interaction with TfR1 was relevant to the transcriptional regulation of p53 target genes. Our results support the positive regulation of nuclear TfR1 on DNA damage repair-related genes, especially for the NER pathway.

2024-12-27 | GSE271110 | GEO

Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation

Project description:Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation

| PRJNA1130079 | ENA

Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation [RNA-seq]

Project description:Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation [RNA-seq]

| PRJNA1129875 | ENA

Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation [RNA-seq]

2024-12-27 | GSE271109 | GEO

Nuclear translocation of TfR1 facilitating tumor progression via p53-mediated gene regulation

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-12-27 | GSE271155 | GEO

Expression data from wildtype and Tfr1 heart KO mice

Project description:We deleted Tfr1 in the heart to determine the role of Tfr1 in iron uptake in normal cardiac funciton We used microarrays to identify global gene changes associated with deletion of Tfr1 in skeletal muscle We isolated RNA from WT and Tfr1 KO hearts at both postnatal day 5 and postnatal day 10.RNA was labaled and hibridized to Affymetrics microarrays.

2015-05-12 | E-GEOD-68745 | biostudies-arrayexpress

Expression data from wildtype and Tfr1 skeletal muscle KO mice

2015-05-08 | GSE68675 | GEO

Expression data from wildtype and Tfr1 heart KO mice

2015-05-12 | GSE68745 | GEO

Expression data from wildtype and Tfr1 skeletal muscle KO mice

Project description:Tfr1 is important for iron uptake in red blood cells. We deleted Tfr1 in skeletal muscle to determine the role of Tfr1 in iron uptake in skeletal muscle. We used microarrays to identify global gene changes associated with deletion of Tfr1 in skeletal muscle We used skeletal muscle and liver from wild type and Tfr1 skeletal muscle KO mice at postnatal day 5 and postnatal day 9. mRNA was extracted from the tissues, labaled and hibridized to Affymetrics microarrays.

2015-05-08 | E-GEOD-68675 | biostudies-arrayexpress

TfR1 binding with H-ferritin nanocarrier achieves prognostic diagnosis and enhances the therapeutic efficacy in clinical gastric cancer

Project description:H-ferritin (HFn) nanocarrier is emerging as a promising theranostic platform for tumor diagnosis and therapy, which can specifically target tumor cells via binding transferrin receptor 1 (TfR1). This led us to investigate the therapeutic function of TfR1 in GC. The clinical significance ofTfR1 was assessed in 178 GC tissues using a magneto-HFn nanoparticle-based immunohistochemistry method. Therapeutic effects of doxorubicin-loaded HFn nanocarriers evaluated on TfR1 positive GC patient-derived xenograft (GC-PDX) models. The biological function of TfR1 was investigated through in vitro and in vivo assays. TfR1 was upregulated (73.03%) in GC tissues and reversely correlated with patient outcome. TfR1 negative sorted cells exhibited tumor-initiating feature, which enhanced tumor formation in vitro and in vivo, migration/invasion, whereas TfR1 positive sorted cells showed significant proliferation ability. Knockout of TfR1 in GC cells also enhanced cell invasion. TfR1 deficient cells displayed immune escape by upregulating PD-L1, CXCL9 and CXCL10, when disposed by IFN-γ. Western blot results demonstrated that knockout of TfR1 in GC cells upregulated Akt and STAT3 signaling. Moreover, in TfR1 positive GC-PDX models, HFn-Dox group significantly inhibited tumor growth and increased mouse survival compared with that of free-Dox group. TfR1 could be a potential prognostic and therapeutic biomarker for GC: (i) TfR1 reversely correlated with patient outcome and its negative cells possess tumor aggressive features; (ii) TfR1 positive cells can be killed by H-ferritin nanocarrier. Given the heterogeneity of GC, HFn nanocarrier combined with other therapies towards TfR1 negative cells (such as: small molecule or immunotherapy etc.) will be new options for GC treatment.

2023-01-01 | GSE143497 | GEO

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