<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Car I</submitter><funding>European Union</funding><funding>Croatian Science Foundation</funding><pagination>12906</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10454476</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(16)</volume><pubmed_abstract>Despite the advancements in targeted therapy for BRAFV600E-mutated metastatic colorectal cancer (mCRC), the development of resistance to BRAFV600E inhibition limits the response rate and durability of the treatment. Better understanding of the resistance mechanisms to BRAF inhibitors will facilitate the design of novel pharmacological strategies for BRAF-mutated mCRC. The aim of this study was to identify novel protein candidates involved in acquired resistance to BRAFV600E inhibitor vemurafenib in BRAFV600E-mutated colon cancer cells using an integrated proteomics approach. Bioinformatic analysis of obtained proteomics data indicated actin-cytoskeleton linker protein ezrin as a highly ranked protein significantly associated with vemurafenib resistance whose overexpression in the resistant</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Ezrin Inhibition Overcomes Acquired Resistance to Vemurafenib in BRAFV600E-Mutated Colon Cancer and Melanoma Cells In Vitro.</pubmed_title><pmcid>PMC10454476</pmcid><funding_grant_id>IP-2018-01-3900</funding_grant_id><funding_grant_id>IP-2018-01-3900 to Mirela Sedić</funding_grant_id><funding_grant_id>Horizon 2020 programme grant agreement ID 823839</funding_grant_id><funding_grant_id>823839</funding_grant_id><pubmed_authors>Car I</pubmed_authors><pubmed_authors>Vasieva O</pubmed_authors><pubmed_authors>Dittmann A</pubmed_authors><pubmed_authors>Pitesa N</pubmed_authors><pubmed_authors>Kraljevic Pavelic S</pubmed_authors><pubmed_authors>Sedic M</pubmed_authors><pubmed_authors>Bockor L</pubmed_authors><pubmed_authors>Grbcic P</pubmed_authors><pubmed_authors>Klobucar M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ezrin Inhibition Overcomes Acquired Resistance to Vemurafenib in BRAFV600E-Mutated Colon Cancer and Melanoma Cells In Vitro.</name><description>Despite the advancements in targeted therapy for BRAFV600E-mutated metastatic colorectal cancer (mCRC), the development of resistance to BRAFV600E inhibition limits the response rate and durability of the treatment. Better understanding of the resistance mechanisms to BRAF inhibitors will facilitate the design of novel pharmacological strategies for BRAF-mutated mCRC. The aim of this study was to identify novel protein candidates involved in acquired resistance to BRAFV600E inhibitor vemurafenib in BRAFV600E-mutated colon cancer cells using an integrated proteomics approach. Bioinformatic analysis of obtained proteomics data indicated actin-cytoskeleton linker protein ezrin as a highly ranked protein significantly associated with vemurafenib resistance whose overexpression in the resistant</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Aug</publication><modification>2026-04-07T15:46:33.088Z</modification><creation>2025-02-19T04:01:06.026Z</creation></dates><accession>S-EPMC10454476</accession><cross_references><pubmed>37629086</pubmed><doi>10.3390/ijms241612906</doi></cross_references></HashMap>