Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Epigenetic suppression of PGC1α (PPARGC1A) causes collateral sensitivity to HMGCR-inhibitors within BRAF-treatment resistant melanomas.

Nature communications - 5 Jun 2023

Liang Jiaxin, Yu Deyang, Luo Chi, Bennett Christopher, Jedrychowski Mark, Gygi Steve P, Widlund Hans R, Puigserver Pere

Abstract excerpt

While targeted treatment against BRAF(V600E) improve survival for melanoma patients, many will see their cancer recur. Here we provide data indicating that epigenetic suppression of PGC1α defines an aggressive subset of chronic BRAF-inhibitor treated melanomas. A metabolism-centered pharmacological screen further identifies statins (HMGCR inhibitors) as a collateral vulnerability within PGC1α-suppressed...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Epigenesis, Genetic
Share to Hydroxymethylglutaryl-CoA Reductase Inhibitors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hydroxymethylglutaryl CoA Reductases

Share to Integrins

Share to Melanoma

Share to Neoplasm Recurrence, Local

Share to Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha

Share to Proto-Oncogene Proteins B-raf

Source

Open in PubMed Open full text

Identifiers

PMID: 37277330
DOI: 10.1038/s41467-023-38968-7
PMCID: PMC10241879

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Epigenetic suppression of PGC1α (PPARGC1A) causes collateral sensitivity to HMGCR-inhibitors within BRAF-treatment resistant melanomas.PMID 37277330Read ↗

BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations.Semantic proximity Read ↗

Disrupting peroxisomes alters lipid metabolism in melanoma and uncovers a novel therapeutic vulnerability in combination with MAPK-targeted therapiesSemantic proximity Read ↗

Cholesterol Regulates the Tumor Adaptive Resistance to MAPK Pathway Inhibition.Semantic proximity Read ↗

The Slow Cycling Phenotype: A Growing Problem for Treatment Resistance in Melanoma.Semantic proximity Read ↗

Reprogramming miRNAs global expression orchestrates development of drug resistance in BRAF mutated melanomaSemantic proximity Read ↗

Simvastatin reprograms lipid metabolism in B16.F10 melanoma cells to favor an early resistant phenotype.Semantic proximity Read ↗

ROS induction as a strategy to target persister cancer cells with low metabolic activity in NRAS mutated melanomaSemantic proximity Read ↗

Increased inflammatory lipid metabolism and anaplerotic mitochondrial activation follow acquired resistance to vemurafenib in BRAF-mutant melanoma cells.Semantic proximity Read ↗

Novel CRISPR-Cas9 BAP1 Knockout Pre-Clinical Tumor Model Recapitulates Human Melanoma Tumorigenesis and Immune EvolutionSemantic proximity Read ↗

Novel CRISPR-Cas9 BAP1 Knockout Pre-Clinical Tumor Model Recapitulates Human Melanoma Tumorigenesis and Immune EvolutionSemantic proximity Read ↗

Sustained SREBP-1-dependent lipogenesis as a key mediator of resistance to BRAF-targeted therapy.Semantic proximity Read ↗

The RhoJ-BAD signaling network: An Achilles' heel for BRAF mutant melanomas.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.