Expression data for HMLE-based EMT models
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE181322 | GEO | 2021/08/03
REPOSITORIES: GEO
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Project description:Expression data for HMLE-based EMT models
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Project description:Immortalized non-cancerous human mammary epithelial cells (HMLE) were transfected to express the murine fusion protein Twist1-estrogen receptor(point mutation G525R) (HTER). Twist1-mediated gene expression is activated by stimulation with 4-hydroxytamoxifen for several days and induces an epithelial-mesenchymal transition (EMT) in HTER cells. In breast cancer, EMT equips cancer cells for metastasis and therapy resistance. As control, HTER cells were treated with vehicle (methanol). As additional controls, HMLE cells were stimulated with 4-hydroxytamoxifen or methanol, respectively. Prior to RNA sequencing, EMT-undergoing HTER cells were sorted by fluorescence-activated cell sorting (FACS) based on E-Cadherin and CD44 surface protein levels into three populations, epithelial (E), hybrid epithelial-mesenchymal (EM), and mesenchymal (M): E-Cadherin_high_CD44_low (E), E-Cadherin_medium_CD44_medium (EM), and E-Cadherin_low_CD44_high (M).
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Project description:Numerous epithelial-to-mesenchymal transition (EMT)-promoting transcription factors have been implicated in tumorigenesis or metastasis, as well as chemoresistance of cancer. However, the underlying mechanism mediating these processes is unclear. Here we report that Foxq1, a forkhead box-containing transcription factor and EMT-inducing gene, promotes stemness traits and chemoresistance in mammary epithelial cells. We identify Twist1, Zeb2, and PDGFRM-NM-1 and M-NM-2 as Foxq1 downstream targets using an expression profiling assay. Further studies reveal that PDGFRM-NM-1 and M-NM-2 can be directly regulated by Foxq1, or indirectly through Twist1. Knockdown of both PDGFRM-NM-1 and M-NM-2 shows more significant effects on reversing Foxq1-promoted oncogenesis in vitro and in vivo than knockdown by either PDGFRM-NM-1 or M-NM-2 alone. PDGFRM-NM-2, but not PDGFRM-NM-1, shows potent effects in reversing Foxq1-promoted stemness traits. Moreover, pharmacological inhibition or gene silencing of PDGFRs sensitize mammary epithelial cells to chemotherapeutic agents in vitro and in vivo. These findings collectively indicate PDGFRs as critical mediators underlying breast cancer tumorigenesis and chemoresistance driven by EMT promoting genes, which have potential clinical implications for cancer therapy. The purpose of these experiments is to investigate the downstream targets of several transcriptional factors including Foxq1 and IRX5. Another purpose is to compare the expression pattern between basal-like breast cancer cells including MDA-MB231, SUM159 and SUM1315.
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Project description:Numerous epithelial-to-mesenchymal transition (EMT)-promoting transcription factors have been implicated in tumorigenesis or metastasis, as well as chemoresistance of cancer. However, the underlying mechanism mediating these processes is unclear. Here we report that Foxq1, a forkhead box-containing transcription factor and EMT-inducing gene, promotes stemness traits and chemoresistance in mammary epithelial cells. We identify Twist1, Zeb2, and PDGFRα and β as Foxq1 downstream targets using an expression profiling assay. Further studies reveal that PDGFRα and β can be directly regulated by Foxq1, or indirectly through Twist1. Knockdown of both PDGFRα and β shows more significant effects on reversing Foxq1-promoted oncogenesis in vitro and in vivo than knockdown by either PDGFRα or β alone. PDGFRβ, but not PDGFRα, shows potent effects in reversing Foxq1-promoted stemness traits. Moreover, pharmacological inhibition or gene silencing of PDGFRs sensitize mammary epithelial cells to chemotherapeutic agents in vitro and in vivo. These findings collectively indicate PDGFRs as critical mediators underlying breast cancer tumorigenesis and chemoresistance driven by EMT promoting genes, which have potential clinical implications for cancer therapy.
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Project description:Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist
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Project description:Snail and Twist are two EMT inducer, expression of Snail or Twist will induce EMT in HMLE and MCF10A cells. By introducing Snail or Twist in HMLE and MCF10A cells, which lack the expression of these two proteins, will identify the genes are induced during EMT. We used microarray analysis to compare the gene expression profiles between the mammamry epithleial cells and the cells undergone EMT.
2020-01-10 | GSE143349 | GEO
Project description:Twist is a key EMT inducer, expression of Twist will induce EMT in HMLE and breast tumor T47D cells By expressing Twist in HMLE and T47D cells, which lack the expression of Twist, will identify the genes regulated by Twist Expressing Twist in HMLE and T47D cells, stable clones were selected and treated with BET inhibitor JQ1 and RNA were prepared for microarray analysis
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Project description:Two engineered HMLE cell lines representing various degrees of EMT were treated with a drug in development to target and inhibit SNAIL interaction with PTP53, called GN-25 total RNA was isolated and analyzed in an Agilent two-color experiment. Four biological replicates of each condition were directly compared, GN25 treated compared to untreated reference The impact of GN-25 on gene expression was investigated using two engineered HMLE cell lines: one stably overexpressing Kras another stably overexpressing Kras and SNAIL
2013-05-31 | E-GEOD-44397 | biostudies-arrayexpress
Project description:Using a TWIST1-inducible epithelial-to-mesenchymal transition (EMT) model in HMLE cells, miRNA changes were profiled at different time points during an active EMT.
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Project description:Epithelial–mesenchymal transition (EMT) is known to be involved in cancer metastasis and pathogenesis. Metabolic re-wiring is now considered to be one of the hallmarks of cancer. In this study, we studied the metabolic changes during EMT in three breast EMT cell models with a proteomic approach. The study showed well-known changes during EMT including CDH1, CDH2, VIM, LGALS1, SERPINE1 and PKP3. It also suggested a list of dysregulated metabolic enzymes: SORD, TSTA3, FDFT1 and UGDH. UGDH had the biggest change and is associated with patient survival. We further studied the role of UGDH in EMT and found out knockdown of UGDH with siRNA can decrease the intracellular glycerophosphocholine level and it can also slow cell proliferation and invasion in mesenchymal cells. Besides, knockdown of UGDH downregulated the expression of a well-known EMT marker, SNAI1. PDGFRB is highly expressed in mesenchymal cells and PDGFD is highly secreted from mesenchymal cells. Knockdown of PDGFRB with siRNA downregulated UGDH potentially via NFkB.
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