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Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [OVCAR8ip1 BARD1 overexpression]

ABSTRACT: Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [OVCAR8ip1 BARD1 overexpression]

PROVIDER: PRJNA1039887 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26816336_1.fastq.gz	Fastqsanger.gz
	SRR26816336_2.fastq.gz	Fastqsanger.gz
	SRR26816337_1.fastq.gz	Fastqsanger.gz
	SRR26816337_2.fastq.gz	Fastqsanger.gz
	SRR26816338_1.fastq.gz	Fastqsanger.gz

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Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [OVCAR8ip1 BARD1 overexpression]

Project description:Despite widespread use of anti-vascular endothelial growth factor (VEGF) antibody (AVA) for cancer therapy, most patients develop progressive disease after initial response. Therefore, novel strategies are needed to understand and overcome AVA resistance. Here, we identify an unexpected role of BRCA1-associated RING domain 1 (BARD1) in overcoming adaptive resistance to AVA. We investigated the effects of epigenetic modulation on cellular response to AVA; in particular, the molecular effects of both global and targeted DNA methylation. Using in vitro assays, BARD1 was identified as being specifically involved in angiogenesis. Sequential treatment with azacytidine overcame AVA therapy resistance in cancer models in vivo. We further demonstrated that specifically targeting BARD1 with either small-interfering RNA or CpG-targeted demethylation reduced tumor growth when combined with AVA therapy (compared with AVA alone) in mouse models of ovarian cancer. These results identify a previously unrecognized role for BARD1 in tumor angiogenesis and show that targeted restoration of BARD1 can enhance the efficacy of AVA therapy in cancer models.

2025-06-16 | GSE247653 | GEO

Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [SKOV3 BARD1 siRNA-RNASeq]

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Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [BeadChip expression]

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Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1

Project description:Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1

| PRJNA1039884 | ENA

Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [SKOV3 BARD1 siRNA-RNASeq]

Project description:Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [SKOV3 BARD1 siRNA-RNASeq]

| PRJNA1039889 | ENA

Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [methylation]

Project description:Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [methylation]

| PRJNA1039888 | ENA

Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [BeadChip expression]

Project description:Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [BeadChip expression]

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Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1 [methylation]

Project description:Genome wide DNA methylation profiling of anti-VEGF resistant SKOV3 tumor samples treated with B20 and/or Azacytidine. The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 450,000 CpGs in SKOV3 tumors. Samples included 2 control IgG, 2 Azacytidine, 2 B20 and 2 B20+Azacytidine treated SKOV3ip1 tumors.

2025-06-17 | GSE247655 | GEO

Overcoming resistance to anti-VEGF therapy via epigenetic regulation of BARD1

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

2025-06-17 | GSE247656 | GEO

Overcoming adaptive resistance to anti-VEGF therapy by targeting CD5L.

Project description:Antiangiogenic treatment targeting the vascular endothelial growth factor (VEGF) pathway is a powerful tool to combat tumor growth and progression; however, drug resistance frequently emerges. We identify CD5L (CD5 antigen-like precursor) as an important gene upregulated in response to antiangiogenic therapy leading to the emergence of adaptive resistance. By using both an RNA-aptamer and a monoclonal antibody targeting CD5L, we are able to abate the pro-angiogenic effects of CD5L overexpression in both in vitro and in vivo settings. In addition, we find that increased expression of vascular CD5L in cancer patients is associated with bevacizumab resistance and worse overall survival. These findings implicate CD5L as an important factor in adaptive resistance to antiangiogenic therapy and suggest that modalities to target CD5L have potentially important clinical utility.

| S-EPMC10133315 | biostudies-literature

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