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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE271109 | GEO | 2024/12/27

REPOSITORIES: GEO

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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

Expression data from wildtype and Tfr1 skeletal muscle KO mice

2015-05-08 | GSE68675 | 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 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 globally regulates transcription and alternative splicing

Project description:In the current study, to figure out the regulation pattern of TfR1, we knocked down TFRC expression level by shRNA in HeLa cells. RNA-sequencing (RNA-seq) was used to analyze the global transcript level and alternative splicing (AS) on knockdown-treated (KD) and normal control (NC) cell samples. 629 differentially expressed genes (DEGs) were identified between OE and NC, and Gene ontology (GO) and KEGG analysis for DEGs were carried out. It was found that multiple DEGs were involved in O-glycan processing, protein modification, response to hypoxia and ATP catabolic process, indicating the down-regulated expression of TfR1 extensively disturbed cell physiology.

2022-05-08 | GSE131598 | GEO

TfR1 extensively regulates the expression of genes associated with ion transport and immunity

Project description:The transferrin receptor 1 (TfR1), encoded by TFRC gene, is the gatekeeper of cellular iron uptake for cells. A variety of molecular mechanisms are at work to tightly regulate TfR1 expression, and abnormal TfR1 expression was associated with diseases. In the current study, to figure out the regulation pattern of TfR1, we cloned and overexpressed human TFRC gene in HeLa cells. RNA-sequencing (RNA-seq) was used to analyze the global transcript level on overexpression-treated (OE) and normal control (NC) cell samples. 1669 differentially expressed genes (DEGs) were identified between OE and NC, and Gene ontology (GO) analysis for DEGs were carried out. It was found that lots of DEGs were associated with ion transmembrane transport and immunity. Moreover, the network was constructed on basis of DEGs regulating ion transport and immunity, the results revealed that TFRC was the node gene of the network, further suggesting that precisely controlled TfR1 expression might be not only essential for iron homeostasis, but also globally important for cell physiology, including ion transport and immunity.

2021-08-27 | GSE130048 | GEO

The yeast GG-NER complex evicts histone H2A.Z-containing barrier nucleosomes from CID boundaries during DNA repair

Project description:Background: Repair of DNA damage requires chromatin remodeling to permit removal of the lesions. How nucleosomes are remodelled to initiate repair of DNA damage remains largely unknown. Here, we describe how chromatin is altered during repair of UV-induced DNA damage at the level of the linear organisation of nucleosomes. Results: Using MNase-seq, we identified a subset of nucleosomes in the genome that are remodelled in UV-damaged wild-type yeast cells. We mapped the genomic location of these nucleosomes, showing that they contain the histone variant H2A.Z. The remodelling observed is consistent with histone exchange or eviction at these positions. This depends on the yeast SWI/SNF global genome nucleotide excision repair (GG-NER) chromatin-remodelling complex. Remarkably, we found that in the absence of DNA damage, the GG-NER complex occupies chromatin at nucleosome free regions separating adjacent nucleosomes. This establishes the nucleosome structure at these genomic locations, which we refer to as GG-NER complex binding sites (GCBS’s). We observed that these sites are frequently located precisely at certain boundary regions that delineate chromasomally interacting domains (CIDs). These boundaries define chromosomal domains of higher-order nucleosome-nucleosome interaction. We demonstrate that the GG-NER complex redistributes following remodelling of these nucleosomes after DNA damage taking up genomic positions located within the CIDs. This permits the efficient removal of DNA damage at these sites. Conclusions: We argue that organising DNA repair in the genome as described may define origins of DNA repair that greatly reduces the genomic search space for DNA damage recognition, thus ensuring the efficient repair of damage in chromatin.

2018-12-06 | E-MTAB-6569 | 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

Role of Set2 in regulating transcription coupled-nucleotide excision repair

Project description:Repair of UV damage from the transcribed strand (TS) of yeast genes is rapid due to the transcription coupled nucleotide excision repair (TC-NER) pathway. TC-NER is triggered when RNA polymerase stalls at UV damage, such as a UV-induced cyclobutane pyrimidine dimer (CPD). During transcription, the histone methyltransferase Set2 methylates histone H3K36, but it is not known if Set2 regulates TC-NER. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lacking Set2.

2022-02-21 | GSE179794 | GEO

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