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Transcriptional regulation by TES and TEAD1 in SNB19 glioblastoma cells: RNA-seq

ABSTRACT: This study investigates transcriptional regulation by TES (TEAD1 Epigenetic Silencer, an engineered epigenetic silencer factor targeting the YAP/TAZ-TEAD axis) in SNB19 glioblastoma cells using RNA-seq. TES was engineered by fusing the KRAB domain, the catalytic domain of DNMT3A together with DNMT3L, and the N-terminal 166 amino acids of TEAD1. RNA-seq was performed 48 hours after lentiviral transduction to identify differentially expressed genes upon TES expression compared to GFP control in three biological replicates per condition. TES expression induced widespread transcriptional repression of YAP/TAZ-dependent gene programs, with downregulated genes enriched for cell-cycle regulation and TEAD family transcription factor binding sites.

ORGANISM(S): Homo sapiens

PROVIDER: GSE319888 | GEO | 2026/02/23

REPOSITORIES: GEO

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Project description:Uncontrolled Transforming growth factor-beta (TGFβ) signaling promotes aggressive metastatic properties in late-stage breast cancers. However, how TGFβ-mediated cues are directed to induce late-stage tumorigenic events is poorly understood, particularly given that TGFβ has clear tumor suppressing activity in other contexts. Here we demonstrate that the transcriptional regulators TAZ and YAP (TAZ/YAP), key effectors of the Hippo pathway, are necessary to promote and maintain TGFβ-induced tumorigenic phenotypes in breast cancer cells. Interactions between TAZ/YAP, TGFβ-activated SMAD2/3, and TEAD transcription factors reveal convergent roles for these factors in the nucleus. Genome-wide expression analyses indicate that TAZ/YAP, TEADs and TGFβ-induced signals coordinate a specific pro-tumorigenic transcriptional program. Importantly, genes cooperatively regulated by TAZ/YAP, TEAD, and TGFβ, such as the novel targets NEGR1 and UCA1, are necessary for maintaining tumorigenic activity in metastatic breast cancer cells. Nuclear TAZ/YAP also cooperate with TGFβ signaling to promote phenotypic and transcriptional changes in non-tumorigenic cells to overcome TGFβ repressive effects. Our work thus identifies crosstalk between nuclear TAZ/YAP and TGFβ signaling in breast cancer cells, revealing novel insight into late-stage disease-driving mechanisms. Expression profiling was conducted following the repression of the transcriptional regulators TAZ and YAP (TAZ/YAP), the TEAD family of transcription factors (TEAD1/2/3/4), or the TGFb signaling pathway (with SB-431542, an inhibitor of the TBRI recpeptor) in human MDA-MB-231-LM2 breast cancer cells treated with TGFβ1. Human MDA-MB-231-LM2-4 breast cancer cells were transfected with control siRNA, or siRNAs targeting TAZ/YAP or all four TEADs and were treated 24 hours later with 500pM TGFβ1 or 5mM SB-431542 for an additional 24 hours. Total RNA was isolated and twelve microarrays in total were performed, with each condition carried out three times on separate days. The Boston University Microarray Core generated the data using the Affymetrix Human Gene 1.0 St Array.

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Transcriptional regulation by TES and TEAD1 in SNB19 glioblastoma cells: RNA-seq

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