Ontology highlight
ABSTRACT:
PROVIDER: PRJNA993382 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25234124_1.fastq.gz | Fastqsanger.gz | |||
| SRR25234124_2.fastq.gz | Fastqsanger.gz | |||
| SRR25234125_1.fastq.gz | Fastqsanger.gz | |||
| SRR25234125_2.fastq.gz | Fastqsanger.gz | |||
| SRR25234126_1.fastq.gz | Fastqsanger.gz |
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Project description:Radioresistance is one of the main factors that lead to the failure of radiotherapy in lung cancer patients. The mechanisms underlying these processes are, however, not fully understood. Here, we find that the low levels of FOXN3 protein is associated with poor prognosis of lung cancer patients. Furthermore, we show that depletion of FOXN3 promotes DNA damage repair and confers lung cancer radioresistance in a BRCA1-dependent manner. Mechanistically, we uncover that E3 ligase β-Trcp and protein kinase RSK2 bind to and cooperatively induce the ubiquitin-mediated degradation of FOXN3. More importantly, β-Trcp and RSK2-mediated ubiquitination of FOXN3 facilitate DNA damage repair in lung cancer. Thus, our findings reveal the molecular mechanism to control the abundance of FOXN3 in DNA damage repair, indicating that targeting β-Trcp/RSK2/FOXN3/BRCA-1 axis may be a novel radiosensitization strategy in lung cancer.
2023-06-30 | GSE218171 | GEO
Project description:The mammalian retina contains a complex mixture of different types of neurons. We find that the microRNA miR-216b is preferentially expressed in postmitotic retinal amacrine cells in the mouse retina, and expression of miR-216a/b and miR-217 in the retina depend in part on Ptf1a, a transcription factor required for amacrine cell differentiation. Surprisingly, ectopic expression of miR-216b, or the related miR-216a, can direct the formation of additional amacrine cells in the developing retina. In addition, we observe the loss of bipolar neurons in the retina after miR-216b expression. We identify the mRNA for the transcriptional regulator Foxn3 as a retinal target of miR-216b by Argonaute PAR-CLIP and reporter analysis. Inhibition of Foxn3 in the postnatal developing retina by RNAi also increases the formation of amacrine cells and reduces bipolar cell formation, while overexpression of Foxn3 inhibits amacrine cell formation prior to the expression of Ptf1a. Disruption of Foxn3 by CRISPR in embryonic retinal explants also reduces amacrine cell formation. Co-expression of Foxn3 partially reverses the effects of ectopic miR-216b on retinal cell type formation. Our results identify Foxn3 as a novel regulator of interneuron formation in the developing retina and suggest that miR-216b likely regulates expression of Foxn3 and other genes in amacrine cells.
2021-12-22 | GSE165831 | GEO
Project description:The mammalian retina contains a complex mixture of different types of neurons. We find that the microRNA miR-216b is preferentially expressed in postmitotic retinal amacrine cells in the mouse retina, and expression of miR-216a/b and miR-217 in the retina depend in part on Ptf1a, a transcription factor required for amacrine cell differentiation. Surprisingly, ectopic expression of miR-216b, or the related miR-216a, can direct the formation of additional amacrine cells in the developing retina. In addition, we observe the loss of bipolar neurons in the retina after miR-216b expression. We identify the mRNA for the transcriptional regulator Foxn3 as a retinal target of miR-216b by Argonaute PAR-CLIP and reporter analysis. Inhibition of Foxn3 in the postnatal developing retina by RNAi also increases the formation of amacrine cells and reduces bipolar cell formation, while overexpression of Foxn3 inhibits amacrine cell formation prior to the expression of Ptf1a. Disruption of Foxn3 by CRISPR in embryonic retinal explants also reduces amacrine cell formation. Co-expression of Foxn3 partially reverses the effects of ectopic miR-216b on retinal cell type formation. Our results identify Foxn3 as a novel regulator of interneuron formation in the developing retina and suggest that miR-216b likely regulates expression of Foxn3 and other genes in amacrine cells.
2021-12-22 | GSE165830 | GEO
Project description:The mammalian retina contains a complex mixture of different types of neurons. We find that the microRNA miR-216b is preferentially expressed in postmitotic retinal amacrine cells in the mouse retina, and expression of miR-216a/b and miR-217 in the retina depend in part on Ptf1a, a transcription factor required for amacrine cell differentiation. Surprisingly, ectopic expression of miR-216b, or the related miR-216a, can direct the formation of additional amacrine cells in the developing retina. In addition, we observe the loss of bipolar neurons in the retina after miR-216b expression. We identify the mRNA for the transcriptional regulator Foxn3 as a retinal target of miR-216b by Argonaute PAR-CLIP and reporter analysis. Inhibition of Foxn3 in the postnatal developing retina by RNAi also increases the formation of amacrine cells and reduces bipolar cell formation, while overexpression of Foxn3 inhibits amacrine cell formation prior to the expression of Ptf1a. Disruption of Foxn3 by CRISPR in embryonic retinal explants also reduces amacrine cell formation. Co-expression of Foxn3 partially reverses the effects of ectopic miR-216b on retinal cell type formation. Our results identify Foxn3 as a novel regulator of interneuron formation in the developing retina and suggest that miR-216b likely regulates expression of Foxn3 and other genes in amacrine cells.
2021-12-22 | GSE165827 | GEO
Project description:We sequenced mRNA from livers of 7 dpf transgenic zebrafish overexpressing foxn3 (in the liver) and non-transgenic siblings
2016-04-10 | GSE80003 | GEO
Project description:Alternative processing of pre-mRNA transcripts is a major source of protein diversity in eukaryotes and has been implicated in several disease processes including cancer. In this study we have performed a genome wide analysis of alternative splicing events with the GeneChip Human Exon 1.0 ST Array from Affymetrix in lung adenocarcinoma. We found that ~13.3% of the 17800 core Refseq genes appear to have alternative transcripts that are differentially expressed in lung adenocarcinoma versus normal. According to their known functions the largest subset of these genes (30.8%) is believed to be cancer related. Detailed analysis was performed for several genes using PCR, quantitative RT-PCR and DNA sequencing. We found overexpression of ERG variant 2 but not variant 1 in lung tumors and overexpression of CEACAM1 variant 1 but not variant 2 in lung tumors but not in breast or colon tumors. We also identified a novel, overexpressed variant of CDH3 and verified the overexpression of a novel variant of P16. These findings demonstrate how analysis of alternative pre-mRNA processing can shed additional light on differences between tumors and normal tissues as well as between different tumor types. Such studies may lead to the development of additional tools for tumor diagnosis, prognosis and therapy. Keywords: Alternative splice analysis of exon data with ANOVA compared tumor and matched normal 20 tumor/normal paired specimens (n=40). Tumor samples are from lung adeno carcinoma whereas normals are from adjacent normal lung tissue.
2008-10-17 | E-GEOD-12236 | biostudies-arrayexpress
Project description:The forkhead box (FOX) family of proteins is composed of more than 50 members that are phylogenetically classified into 19 subclasses (A to S). These transcription factors all share a homology in their DNA-binding domain, the forkhead domain, also known as winged helix due to its butterfly-like structural appearance.FOX proteins have been implicated in a broad spectrum of cellular processes including cell proliferation, differentiation, DNA repair, metabolism, and aging. However, the biological function of the mammalian forkhead transcription factors of the N class including FOXN3 remains to be investigated. The SIN3A complex is a large protein assembly consisting of over a dozen of proteins including SIN3A, HDAC1/2, RBBP4/7 and etc. This complex is recruited by multiple transcription repressors and impacts on multifaceted biological functions ranging from development, differentiation, and senescence to oncogenic transformation. Long noncoding RNAs (lncRNAs) are a class of noncoding RNAs that are over 200 nucleotides in length. In the past years, these molecules have emerged as important components of the epigenetic regulatory network to influence transcription as well as other nuclear activities, and their dysregulation underlies several pathologic states including cancer. One of the lncRNAs, NEAT1 (nuclear paraspeckle assembly transcript 1), is a highly abundant lncRNA initially described as a structural component of nuclear paraspeckles. Subsequent studies suggest that NEAT1 also influences transcription through either an indirect mechanism or a direct way. In this study, we investigated the function and the underlying mechanism of FOXN3 in breast cancer cells. We showed that FOXN3 is physically associated with the SIN3A complex and identified that NEAT1, which is induced by estrogen in breast cancer cells, is required for this interaction. We analyzed the genomic targets of the FOXN3/SIN3A/NEAT1 complex and demonstrated that estrogen receptor (ER) itself is regulated, through negative feedback, by the FOXN3/SIN3A/NEAT1 complex. We investigated the role of the FOXN3/SIN3A/NEAT1 complex in breast cancer metastasis and explored the clinicopathological significance of the ER-NEAT1-FOXN3/NEAT1/SIN3A-GATA3 axis in breast cancer.
2017-06-01 | GSE93780 | GEO
Project description:We performed global gene expression profiling of transgenic rat brain and testis tissues using mRNA sequencing (mRNA-seq) to investigate the impact of epigenetic modifier overexpression on tissue gene expression patterns.
2021-03-01 | GSE128777 | GEO
Project description:Background: MicroRNAs (miRNAs) are small noncoding RNAs about 22 nucleotides in length and regulate mRNA expression by binding to 3?UTR of mRNAs and causing translation repression or degradation of mRNAs. Recent studies have revealed that microRNAs play important regulatory roles in carcinogenesis. However, the complement of miRNAs involved in lung carcinogenesis and tumor biology is generally unknown. We used high-throughput sequencing technology to investigate miRNA expression profiles in a study of paired lung non-small cell carcinomas and remote noncancerous lung tissues. Methods: Total RNA was isolated by Trizol from patient lung tissues, including 1 non-pair of macroscopic lung adenocarcinoma tissue, and 20 pairs of macroscopic lung adenocarcinoma tissues and corresponding paired noncancerous lung tissues from the same patients, 1 non-pair of noncancerous lung tissues of squamous cell carcinoma patient, and 10 pairs of squamous cell carcinoma and corresponding paired noncancerous lung tissues from the same patients. Small RNA library of each total RNA was constructed with Illumina?s Small RNA Sample Prep Kit, followed by high-throughput sequencing. Statistical differences in microRNA expression between groups were analyzed by GenePattern software. Results: Using 2-fold threshold with FDR<0.05, there were ~90 miRNAs differentiated the lung cancers from nontumor lung tissues, both histologies. (a) The sets of microRNAs differentiating adenocarcinoma from paired nontumor tissues are largely different from those differentiating squamous tumors. There were 40 upregulated and 23 downregulated microRNAs differentiating adenocarcinoma Tvs.NT . For squamous cell, the numbers were 19 and 6, respectively. (b) In common between the two tumor histologies, there were six common upregulated microRNAs (miR-21, 135b, 200a, 494, 708. 1259), and four common down-regulated microRNAs (miR-144, 184, 516a, 1251). (c) Comparing our 22 miRNAs in common with Yanaihara/Harris Cancer Cell 2006 using spotted microarrays, we found similar direction of change in 19/22. (d) As a group, the top over-expressed miRNA in lung tumors (determined as fold change > 2, and comprising at least .01% of total miRNA) are able to predict mRNAs that are differentially expressed in those same samples (p=4.6x10^-6). Conclusions: This effort represents one of the more comprehensive surveys of the lung tumor micronome. (i) Tumor microRNA complement differs from far-adjacent lung; (ii) Histologies differ in their overall, and tumor-distinctive microRNA complement; (iii) Statistical correlations of individual microRNA:mRNA (putative) pairing from the same tissue sets are pending. (iv) Experimental confirmation of microRNA:mRNA targeting, using our microRNA affinity pull down assay is also pending.
2012-03-31 | GSE33858 | GEO