Gene expression profile of WT and mdig/mina53 KO MDA-MB 231 breast cancer cells [RNA-Seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE282125 | GEO | 2026/01/20
REPOSITORIES: GEO
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Project description:The mineral dust-induced gene (mdig, also called as MINA or RIOX2) is upregulated in breast cancer and predicts poor overall survival of breast cancer patients. Our studies suggested the anti-metastasis feature of mdig in regulating the cell motility of breast cancer cells. Here we studied the transcriptomic profile of human triple negative breast cancer cells MDA-MB-231 that were knocked out for mdig via CRISPR-Cas 9 gene editing. Our analysis identified distinct transcriptomic profiles in mdig knockout cells, where genes associated with epithelial-mesenchymal transition (EMT) and TGF-β pathways were upregulated
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Project description:The mineral dust-induced gene (mdig, also called as MINA or RIOX2) is overexpressed in breast cancer and its high expression correlates with poor overall survival of the patients. Our studies suggested its role in cell motility, invasion and in the demethylation of DNA and histone proteins. Here we studied the global histone methylation profiles of human triple negative breast cancer cells MDA-MB-231 that were knocked out for mdig via CRISPR-Cas 9 gene editing. Altered histone methylation profiles impacted the transcriptional status of key genes implicated in cell growth, motility, invasion and cancer.
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Project description:Cancer-associated stroma (CAS) profoundly influences development and progression of tumours including mammary carcinoma (mCA). Spontaneous canine simple mCA represent relevant models of human mCA, notably also with respect to CAS reprogramming. While transcriptomic changes in CAS of mCA are well described, it remains unclear to what extent these differences translate to the protein level. Therefore, we sought to gain insight into the proteomic changes in CAS and compare them with transcriptomic changes in the same tissue. To this end, we analysed CAS and matched normal stroma isolated by laser-capture microdissection (LCM) by LC-MS/MS in a cohort of 14 Formalin-fixed paraffin embedded (FFPE) canine mCAs that we had previously characterized using LCM-RNAseq. Our results reveal clear differences in protein abundance between CAS and normal stroma, which are characterised by changes in the extracellular matrix, the cytoskeleton, and cytokines such as TNF. While the proteomics-based analysis of LCM-FFPE tissue detects fewer targets than RNAseq, the protein and RNA levels show a decent degree of correlation, especially for the most deregulated targets. Moreover, the results from both approaches reveal a comparable picture with regards to pathway activation. Finally, we validate transcriptomic upregulation of LTBP2, IGFBP2, COL6A5, POSTN, FN1, COL4A1, COL12A1, PLOD2, COL4A2, and IGFBP7 in CAS on the protein level and demonstrate their adverse prognostic value for human breast cancer. Given the relevance of canine mCA as model for the human disease, our analysis substantiates these targets as disease-promoting stromal components with implications for breast cancer in both humans and dogs.
2021-03-30 | PXD023023 | Pride
Project description:The mineral dust-induced gene (mdig) is overexpressed in a number of human cancers, suggesting critical roles of this gene played on the pathogenesis of cancers. Unlike several other JmjC-domain containing proteins that exhibit histone demethylase activity, it remains enigmatic whether mdig is involved in the demethylation processes of the histone proteins. To provide direct evidence suggesting contribution of mdig to the demethylation of histone proteins, we report the global histone methylation profile of H3K4me3, H3K27me3, H3K9me3, and H3R8me2a in human bronchial epithelial BEAS-2B cells with mina53/mdig knockout. ChIP-seq revealed a pronounced increase of the repressive histone trimethylation with mdig depletion, including H3K9me3 and H3K27me3. Data from both ChIP-seq and RNA-seq suggested that genetic disruption of mdig enriches repressive histone trimethylation and inhibits expression of target genes in the oncogenic pathways of cell growth, stemness of the cells, tissue fibrosis, and cell motility. Our study provides the first insight into the molecular effects of mdig as an antagonist for repressive histone methylation markers and suggests that targeting mdig may represent a new area to explore in cancer therapy.
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Project description:Since bone metastatic breast cancer is an incurable disease, causing significant morbidity and mortality, understanding of the underlying molecular mechanisms would be highly valuable. Here, we describe in vitro and in vivo evidence for the importance of serine biosynthesis in the metastasis of breast cancer to bone. We first characterized the bone metastatic propensity of the MDA-MB-231(SA) cell line variant as compared to the parental MDA-MB-231 cells by radiographic and histological observations in the inoculated mice. Genome-wide gene expression profiling of this isogenic cell line pair revealed that all the three genes involved in the L-serine biosynthesis pathway, phosphoglycerate dehydrogenase (PHGDH), phosphoserine aminotransferase 1 (PSAT1), and phosphoserine phosphatase (PSPH) were upregulated in the highly metastatic variant. This pathway is the primary endogenous source for L-serine in mammalian tissues. Consistently, we observed that the proliferation of MDA-MB-231(SA) cells in serine-free conditions was dependent on PSAT1 expression. In addition, we observed that L-serine is essential for the formation of bone resorbing human osteoclasts and may thus contribute to the vicious cycle of osteolytic bone metastasis. High expression of PHGDH and PSAT1 in primary breast cancer was significantly associated with decreased relapse-free and overall survival of patients and malignant phenotypic features of breast cancer. In conclusion, high expression of serine biosynthesis genes in metastatic breast cancer cells and the stimulating effect of L-serine on osteoclastogenesis and cancer cell proliferation indicate a functionally critical role for serine biosynthesis in bone metastatic breast cancer and thereby an opportunity for targeted therapeutic interventions. Parental MDA-MB-231 cells and MDA-MB-231(SA) cells were cultured in cell culture flasks. RNA was isolated in order to compare the gene expression profiles of these cell variants. Total of two samples. No replicates.
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Project description:We discovered that HnRNPF is significantly upregulated in breast cancer tissues and is closely associated with the cell proliferation signaling pathway. Overexpression of HnRNPF notably inhibits cell proliferation in MDA-MB-231 breast cancer cells. HnRNPF promotes the expression of the cell cycle inhibitor p21.
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Project description:Since bone metastatic breast cancer is an incurable disease, causing significant morbidity and mortality, understanding of the underlying molecular mechanisms would be highly valuable. Here, we describe in vitro and in vivo evidence for the importance of serine biosynthesis in the metastasis of breast cancer to bone. We first characterized the bone metastatic propensity of the MDA-MB-231(SA) cell line variant as compared to the parental MDA-MB-231 cells by radiographic and histological observations in the inoculated mice. Genome-wide gene expression profiling of this isogenic cell line pair revealed that all the three genes involved in the L-serine biosynthesis pathway, phosphoglycerate dehydrogenase (PHGDH), phosphoserine aminotransferase 1 (PSAT1), and phosphoserine phosphatase (PSPH) were upregulated in the highly metastatic variant. This pathway is the primary endogenous source for L-serine in mammalian tissues. Consistently, we observed that the proliferation of MDA-MB-231(SA) cells in serine-free conditions was dependent on PSAT1 expression. In addition, we observed that L-serine is essential for the formation of bone resorbing human osteoclasts and may thus contribute to the vicious cycle of osteolytic bone metastasis. High expression of PHGDH and PSAT1 in primary breast cancer was significantly associated with decreased relapse-free and overall survival of patients and malignant phenotypic features of breast cancer. In conclusion, high expression of serine biosynthesis genes in metastatic breast cancer cells and the stimulating effect of L-serine on osteoclastogenesis and cancer cell proliferation indicate a functionally critical role for serine biosynthesis in bone metastatic breast cancer and thereby an opportunity for targeted therapeutic interventions.
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Project description:We discovered that USP30-AS1 is significantly upregulated in breast cancer tissues and is closely associated with the cell proliferation signaling pathway. Knockdown of USP30-AS1 notably inhibits cell proliferation in MDA-MB-231 breast cancer cells. USP30-AS1 inhibits the expression of the cell cycle inhibitor p21.
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Project description:Post-transcriptional control of mRNAs by RNA-binding proteins (RBPs) has a prominent role in the regulation of gene expression. RBPs interact with mRNAs to control their biogenesis, splicing, transport, localization, translation, and stability. Defects in such regulation can lead to a wide range of human diseases from neurological disorders to cancer. Many RBPs are conserved between Caenorhabditis elegans and humans, and several are known to regulate apoptosis in the adult C. elegans germ line. How these RBPs control apoptosis is, however, largely unknown. Here, we identify mina-1(C41G7.3) in a RNA interference-based screen as a novel regulator of apoptosis, which is exclusively expressed in the adult germ line. The absence of MINA-1 causes a dramatic increase in germ cell apoptosis, a reduction in brood size, and an impaired P granules organization and structure. In vivo crosslinking immunoprecipitation experiments revealed that MINA-1 binds a set of mRNAs coding for RBPs associated with germ cell development. Additionally, a system-wide analysis of a mina-1 deletion mutant compared to wild type, including quantitative proteome and transcriptome data, hints to a post-transcriptional regulatory RBP network driven by MINA-1 during germ cell development in C. elegans. In particular, we found that the germline-specific Argonaute WAGO-4 protein levels are increased in the mina-1 mutant background. Phenotypic analysis of double mutant mina-1;wago-4 revealed that contemporary loss of MINA-1 and WAGO-4 strongly rescues the phenotypes observed in the mina-1 mutant background. To strengthen this functional interaction, we found that upregulation of WAGO-4 in mina-1 mutant animals causes hypersensitivity to exogenous RNAi. Our comprehensive experimental approach allowed us to describe a phenocritical interaction between two RBPs controlling germ cell apoptosis and exogenous RNAi. These findings broaden our understanding of how RBPs can orchestrate different cellular events such as differentiation and death in C. elegans.
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