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

Metformin accelerates the growth of BRAF V600E-driven melanoma by upregulating VEGF-A.

Cancer discovery - 1 Apr 2012

Martin Matthew J, Hayward Robert, Viros Amaya, Marais Richard

Abstract excerpt

UNLABELLED: The antidiabetic drug metformin has antitumor activity in a variety of cancers because it blocks cell growth by inhibiting TORC1. Here, we show that melanoma cells that are driven by oncogenic BRAF are resistant to the growth-inhibitory effects of metformin because RSK sustains TORC1 activity even when AMP-activated protein kinase (AMPK) is activated. We further show that AMPK targets the...

Read the complete abstract on PubMed

Topics

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

Share to AMP-Activated Protein Kinases
Share to Drug Synergism
Share to Extracellular Signal-Regulated MAP Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Imidazoles

Share to Indazoles

Share to Metformin

Share to Ribosomal Protein S6 Kinases

Share to Xenograft Model Antitumor Assays

Source

Open in PubMed Open full text

Identifiers

PMID: 22576211
DOI: 10.1158/2159-8290.CD-11-0280
PMCID: PMC3364710

Genes

BRAF
DUSP6

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Metformin accelerates the growth of BRAF V600E-driven melanoma by upregulating VEGF-A.PMID 22576211Read ↗

Overcoming Resistance to Therapies Targeting the MAPK Pathway in BRAF-Mutated TumoursSemantic proximity Read ↗

Phosphorylation of BRAF by AMPK impairs BRAF-KSR1 association and cell proliferation.Semantic proximity Read ↗

Overcoming Chemoresistance to Vemurafenib in Melanoma via Targeted Inhibition of PCK1 Using 3-mercaptopropionic AcidSemantic proximity Read ↗

BRAF V600E inhibition stimulates AMP-activated protein kinase-mediated autophagy in colorectal cancer cells.Semantic proximity Read ↗

RSK2 promotes melanoma cell proliferation and vemurafenib resistance via upregulating cyclin D1Semantic proximity Read ↗

TORC1 suppression predicts responsiveness to RAF and MEK inhibition in BRAF-mutant melanoma.Semantic proximity Read ↗

SLC36A1-mTORC1 signaling drives acquired resistance to CDK4/6 inhibitorsSemantic proximity Read ↗

BRAFV600E negatively regulates the AKT pathway in melanoma cell lines.Semantic proximity Read ↗

mTORC1 activation blocks BrafV600E-induced growth arrest but is insufficient for melanoma formation.Semantic proximity Read ↗

Co-targeting BRAF and cyclin dependent kinases 4/6 for BRAF mutant cancers.Semantic proximity Read ↗

Sorafenib synergizes with metformin in NSCLC through AMPK pathway activation.Semantic proximity Read ↗

Suppression of Spry1 reduces HIF1α-dependent glycolysis and impairs angiogenesis in BRAF-mutant cutaneous melanoma.Semantic proximity Read ↗

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