ArticleJournal of molecular medicine (Berlin, Germany)2026
MEK inhibitor cobimetinib increases calreticulin and induces immune modulation in TNBC.
Article in Journal of molecular medicine (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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11 authors.
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Abstract
Immunogenic cell death (ICD) can activate immune cells and potentiate the response to immunotherapy. The mitogen-activated protein kinase (MAPK) signaling pathway regulates the immune response and mediates T-cell receptor signaling. Activation of the MAPK signaling pathway decreases the levels of tumor-infiltrating lymphocytes in triple-negative breast cancer (TNBC) and is associated with worse survival. Here, we investigated the potential of the MEK inhibitor cobimetinib as an ICD inducer in TNBC. We demonstrated that cobimetinib elicited hallmarks of ICD, including elevated levels of damage-associated molecular patterns. Ectopic ERK expression attenuated cobimetinib-induced CRT. Cobimetinib also evoked caspase-8 activation with increased Bax and Bak expression, while caspase inhibitor suppressed cobimetinib-induced CRT expression and apoptosis. In immunocompetent (BALB/c) mice bearing 4T1 tumors, cobimetinib exhibited stronger tumor growth inhibition than in immunodeficient (nude) mice, suggesting an immune-dependent antitumor effect. Furthermore, cobimetinib treatment increased the proportions of naïve CD8
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