ArticlebioRxiv : the preprint server for biology2026
IL-6R blockade with tocilizumab disrupts pericyte- and tumor cell-driven IL-6/STAT3 signaling, enhancing docetaxel efficacy in ER+ breast cancer.
Article in bioRxiv : the preprint server for biology, 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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Authors and funding
8 authors.
Funding
Abstract
Metastatic breast cancer is a global health concern with a persistently low five-year survival rate. Taxane microtubule stabilizers, including docetaxel (DTX), are the standard of care in various treatment protocols. DTX is used both as a single agent and in combination therapies, with a majority of ER+ breast cancer patients ultimately developing chemoresistance. The mechanisms contributing to chemoresistance involving the tumor microenvironment (TME) have not been fully elucidated. Specifically, the role of vascular cells within the TME, particularly pericytes, is understudied, and their role in promoting chemoresistance remains unknown. Inflammatory cytokines such as interleukin 6 (IL-6) are known to drive drug resistance via activation of the pro-survival JAK/STAT pathway. We found that DTX induced IL-6 secretion of pericytes by at least two-fold compared to vehicle-treated controls
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Registered trials
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