SEMA6A/RhoA/YAP axis mediates tumor-stroma interactions and prevents response to dual BRAF/MEK inhibition in BRAF-mutant melanoma.

doi:10.1186/s13046-022-02354-w

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

Community

Back to search

Article

SEMA6A/RhoA/YAP axis mediates tumor-stroma interactions and prevents response to dual BRAF/MEK inhibition in BRAF-mutant melanoma.

Journal of experimental & clinical cancer research : CR - 19 Apr 2022

Loria Rossella, Laquintana Valentina, Scalera Stefano, Fraioli Rocco, Caprara Valentina, Falcone Italia, Bazzichetto Chiara, Di Martile Marta, Rosanò Laura, Del Bufalo Donatella, Bossi Gianluca, Sperduti Isabella, Terrenato Irene, Visca Paolo, Soddu Silvia, Milella Michele, Ciliberto Gennaro, Falcioni Rita, Ferraresi Virginia, Bon Giulia

Abstract excerpt

BACKGROUND: Despite the promise of dual BRAF/MEK inhibition as a therapy for BRAF-mutant (BRAF-mut) melanoma, heterogeneous responses have been observed in patients, thus predictors of benefit from therapy are needed. We have previously identified semaphorin 6A (SEMA6A) as a BRAF-mut-associated protein involved in actin cytoskeleton remodeling. The purpose of the present study is to dissect the role of SEMA6A in...

Read the complete abstract on PubMed

Topics

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

Share to Antineoplastic Combined Chemotherapy Protocols

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Melanoma

Share to Mitogen-Activated Protein Kinase Kinases

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins B-raf

Share to rhoA GTP-Binding Protein

Share to Semaphorins

Share to Tumor Microenvironment

Source

Open in PubMed Open full text

Identifiers

PMID: 35440004
DOI: 10.1186/s13046-022-02354-w
PMCID: PMC9016967

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SEMA6A/RhoA/YAP axis mediates tumor-stroma interactions and prevents response to dual BRAF/MEK inhibition in BRAF-mutant melanoma.PMID 35440004Read ↗

Sema6A and Mical1 control cell growth and survival of BRAFV600E human melanoma cells.Semantic proximity Read ↗

Bidirectional cross talk between patient‐derived melanoma and cancer‐associated fibroblasts promotes invasion and proliferationSemantic proximity Read ↗

Tumorigenesis driven by the BRAF <sup>V600E</sup> oncoprotein requires secondary mutations that overcome its feedback inhibition of migration and invasionSemantic proximity Read ↗

Emerging role of ARHGAP29 in melanoma cell phenotype switching.Semantic proximity Read ↗

Vemurafenib and trametinib reduce expression of CTGF and IL-8 in V600EBRAF melanoma cells.Semantic proximity Read ↗

A Feed-Forward Mechanosignaling Loop Confers Resistance to Therapies Targeting the MAPK Pathway in BRAF-Mutant Melanoma.Semantic proximity Read ↗

The Role of Melanoma Cell-Stroma Interaction in Cell Motility, Invasion, and MetastasisSemantic proximity Read ↗

Oncogenic BRAF-Mediated Melanoma Cell InvasionSemantic proximity Read ↗

Tumorigenesis Driven by BRAFV600E Requires Secondary Mutations That Overcome Its Feedback Inhibition of RAC1 and Migration.Semantic proximity Read ↗

Oncogenic B-Raf signaling in melanoma cells controls a network of microRNAs with combinatorial functions.Semantic proximity Read ↗

Upregulated expression of miR-4443 and miR-4488 in drug resistant melanomas promotes migratory and invasive phenotypes through downregulation of intermediate filament nestin.Semantic proximity Read ↗

TRIM9 switches the morphological phenotype of melanoma cellsSemantic proximity Read ↗

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