Phenotype switching in highly invasive resistant to vemurafenib and cobimetinib melanoma cells.

ABSTRACT:

Background

A mutation in the BRAF (serine/threonine-protein kinase B-raf) gene is most often responsible for the progression of melanoma. A breakthrough in its treatment was the application of BRAF and MEK (mitogen-activated protein kinase kinase) inhibitors. Unfortunately, the effectiveness of this therapy is limited due to rapidly emerging resistance to the drugs. We derived two melanoma cell lines resistant to vemurafenib (a BRAF inhibitor)/cobimetinib (an MEK inhibitor). Due to the significant impact of invasion on cancer progression, we focused our further research on this process.

Methods

Cell migration and invasion were assessed via the scratch wound assay. Selected proteins' level as well as the activation of focal adhesion kinase (FAK) were evaluated using Western b

SUBMITTER: Simiczyjew A 

PROVIDER: S-EPMC12542628 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature