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VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 1]

ABSTRACT: To investigate if the drug verteporfin can inhibit VGLL1 co-transcriptional activity in Fulvestrant resistant breast cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE216526 | GEO | 2023/12/05

REPOSITORIES: GEO

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VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 3]

Project description:To investigate the function of VGLL1 in breast cancer and its role in the resistance to endocrine therapies we generated stable MCF7 cells overexpressing VGLL1 using CRISPR/Cas9 Synergistic Activation Mediator (SAM) method (MCF7 ActCas9-VGLL1 cells). MCF7 ActCas9-VGLL1 cells were also cultured in the presence of fulvestrant 100nmM or 1µM to develop fulvestrant resistant cells (MCF7 ActCas9-VGLL1-FULVR) and RNA-seq was performed in the different cell lines.

2023-12-05 | GSE216528 | GEO

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [ChIP-Seq]

Project description:The transcriptional activity of the TEAD4 trascription factor requires co-activators. In this study we found that the expression of the TEAD coactivator VGLL1 is repressed in estrogen receptor positive breast cancer but upon resistance to endocrine threapies VGLL1 is expressed to high levels. To elucidate the importance of the coactivator VGLL1 in breast cancer cells resistant to endocrine therapies and to identify the VGLL1 target genes, we performed ChIP-seq for VGLL1 in MCF7 breast cancer cells resistant to fulvestrant (FULVR) and ChiP-seq for TEAD4 in FULVR cells and the isogenic MCF7 cells.

2023-12-05 | GSE216525 | GEO

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 2]

Project description:To identify VGLL1 target genes we performed RNA-seq following siRNA-mediated VGLL1 downregulation in FULVR cells.

2023-12-05 | GSE216527 | GEO

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer

Project description:VGLL1 drives therapy resistance in estrogen receptor positive breast cancer

| PRJNA894162 | ENA

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [ChIP-Seq]

Project description:VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [ChIP-Seq]

| PRJNA894166 | ENA

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-12-05 | GSE216530 | GEO

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 3]

Project description:VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 3]

| PRJNA894163 | ENA

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 2]

Project description:VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 2]

| PRJNA894164 | ENA

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 1]

Project description:VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [RNA-Seq 1]

| PRJNA894165 | ENA

Placental co-transcriptional activator Vestigial-like 1 (VGLL1) drives tumorigenesis via increasing transcription of proliferation and invasion genes [RNA-seq]

Project description:Vestigial-like 1 (VGLL1) is a co-transcriptional activator that binds to TEA domain-containing transcription factors (TEADs). Its expression is upregulated in a variety of aggressive cancer types, including pancreatic and basal-like breast cancer, and increased transcription of VGLL1 is strongly correlated with poor prognosis and decreased overall patient survival. In normal tissues, VGLL1 is most highly expressed within placental trophoblast cells, which share the common attributes of rapid cellular proliferation and invasion with tumor cells. The impact of VGLL1 in cancer has not been fully elucidated and no VGLL1-targeted therapy currently exists. The aim of this study was to evaluate the cellular function and downstream genomic targets of VGLL1 in placental, pancreatic, and breast cancer cells. Functional assays were employed to assess the role of VGLL1 in cellular invasion and proliferation, and ChIP-seq and RNA-seq assays were performed to identify VGLL1 target genes and potential impact using pathway analysis. ChIP-seq analysis identified eight transcription factors with a VGLL1-binding motif that were common between all three cell types, including TEAD1-4, AP-1, and GATA6, and revealed ~3,000 shared genes with which VGLL1 interacts. Furthermore, increased VGLL1 expression led to an enhancement of cell invasion and proliferation, which was supported by RNA-seq analysis showing transcriptional changes in several genes known to be involved in these processes. This work expands our mechanistic understanding of VGLL1 function in tumor cells and provides a strong rationale for developing VGLL1-targeted therapies for treating cancer patients.

2024-05-25 | GSE267818 | GEO

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