Ontology highlight
ABSTRACT:
PROVIDER: PRJNA272580 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:microRNA expression profile of MCF7 cells with retroviral inducible expression of ΔNp63α [miRNA]
| PRJNA272581 | ENA
Project description:mRNA expression profile of MCF7 cells with retroviral inducible expression of ΔNp63α [total RNA]
| PRJNA272582 | ENA
Project description:MCF7 is a breast adenocarcinoma cell line which exhibits properties of differentiated luminal epithelial cells. ΔNp63α, an N-terminally truncated isoform of p51/p63 protein, plays a critical role in mammary gland development. Here, we inducibly express ΔNp63α in MCF7 cells and studied its role in stemness of breast cancer cells.
2015-12-28 | GSE64954 | GEO
Project description:MCF7 is a breast adenocarcinoma cell line which exhibits properties of differentiated luminal epithelial cells. ΔNp63α, an N-terminally truncated isoform of p51/p63 protein, plays a critical role in mammary gland development. Here, we inducibly express ΔNp63α in MCF7 cells and studied its role in stemness of breast cancer cells.
2015-12-28 | GSE64953 | GEO
Project description:Hypoxia is the most prominent feature in human solid tumors and induces activation of hypoxia-inducible factors and their downstream genes to promote cancer progression. However, whether and how hypoxia regulates overall mRNA homeostasis is unclear. Here we show that hypoxia inhibits global-mRNA decay in cancer cells. Mechanistically, hypoxia induces the interaction of AGO2 with HOIL-1L/HOIP, two crucial components of a linear ubiquitin chain assembly complex, which co-localizes with miRNA-induced silencing complex and in turn catalyzes AGO2 occurring Met1-linked linear ubiquitination (M1-Ubi). A series of biochemical experiments reveal that M1-Ubi of AGO2 restrains miRNA-mediated gene silencing. Moreover, combination analyses of the AGO2-associated mRNA transcriptome by RIP-Seq and the mRNA transcriptome by RNA-Seq confirm that AGO2 M1-Ubi interferes miRNA-targeted mRNA recruiting to AGO2, and thereby facilitates accumulation of global mRNAs. By this mechanism, short-term hypoxia may protect overall mRNAs and enhances stress tolerance, whereas long-term hypoxia in tumor cells results in seriously changing the entire gene expression profile to drive cell malignant evolution.
2021-04-06 | PXD021722 |
Project description:To determine the impact of ΔNp63α knockdown on steady-state mRNA levels, we performed poly(A)-enriched RNA-seq analysis of lung squamous cell carcinoma line H226 (inducible shControl and shp63) in the presence of 1µg/mL doxycycline to induce shRNA expression.
2018-08-27 | GSE111619 | GEO
Project description:MicroRNA (miRNA/miR) miR526b and miR655 overexpressed tumor cell-free secretions promote breast cancer phenotypes in the tumor microenvironment (TME). However, the mechanisms of miRNA regulating TME have never been investigated. With mass spectrometry analysis of MCF7-miRNA-overexpressed versus miRNA-low MCF7-Mock tumor cell secretomes, we identified 34 novel secretory proteins coded by eight genes YWHAB, TXNDC12, MYL6B, SFN, FN1, PSMB6, PRDX4, and PEA15 those are differentially regulated. We used bioinformatic tools and systems biology approaches to identify these markers’ role in breast cancer. Gene ontology analysis showed that the top functions are related to apoptosis, oxidative stress, membrane transport, and motility, supporting miRNA-induced phenotypes. These secretory markers expression is high in breast tumors, and a strong positive correlation exists between upregulated markers’ mRNA expressions with miRNA cluster expression in luminal A breast tumors. Gene expression of secretome markers is higher in tumor tissues compared to normal samples, and immunohistochemistry data supported gene expression data. Moreover, both up and downregulated marker expressions are associated with breast cancer patient survival. miRNA regulates these marker protein expressions by targeting transcription factors of these genes. Premature miRNA (pri-miR526b and pri-miR655) are established breast cancer blood biomarkers. Here we report novel secretory markers upregulated by miR526b and miR655 (YWHAB, MYL6B, PSMB6, and PEA15) are significantly upregulated in breast cancer patients’ plasma, and are potential breast cancer biomarkers.
2023-05-10 | PXD031771 | Pride
Project description:Intervention type:DRUG. Intervention1:Huaier, Dose form:GRANULES, Route of administration:ORAL, intended dose regimen:20 to 60/day by either bulk or split for 3 months to extended term if necessary. Control intervention1:None.
Primary outcome(s): For mRNA libraries, focus on mRNA studies. Data analysis includes sequencing data processing and basic sequencing data quality control, prediction of new transcripts, differential expression analysis of genes. Gene Ontology (GO) and the KEGG pathway database are used for annotation and enrichment analysis of up-regulated genes and down-regulated genes.
For small RNA libraries, data analysis includes sequencing data process and sequencing data process QC, small RNA distribution across the genome, rRNA, tRNA, alignment with snRNA and snoRNA, construction of known miRNA expression pattern, prediction New miRNA and Study of their secondary structure Based on the expression pattern of miRNA, we perform not only GO / KEGG annotation and enrichment, but also different expression analysis.. Timepoint:RNA sequencing of 240 blood samples of 80 cases and its analysis, scheduled from June 30, 2022..
| 2612481 | ecrin-mdr-crc
Project description:In the present study, we established MYC-overexpressing limbal epithelial stem cell line (oeMYC-LESC) that exhibits a biomarker expression profile resembling that of limbal progenitor cells (LPCs). The self-renewal capacity of oeMYC-LESCs was markedly enhanced compared to high-passage cells, primarily through lactylation-dependent mechanisms. Specifically, H3K18la upregulates ΔNp63α, a key transcriptional regulator essential for epithelial stem cell function and the maintenance of stratified epithelial integrity [a]. In vivo studies further demonstrated that the H3K18la‑ΔNp63α axis promotes corneal epithelial regeneration.
2026-01-14 | GSE315524 | GEO