ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Molecular Targets and Therapeutics
This article is part of the Research TopicInnovative Strategies for the Discovery of New Therapeutic Targets in Cancer TreatmentView all 13 articles
Mechanistic Role of CD82 Palmitoylation in Augmenting Antitumor Drug Sensitivity via Apoptosis Regulation
Provisionally accepted
Lanyan Li1Yaning Yu1Sirui Chen1Yihuan Zhang1Can Zhang1Xinyu Yao1Hongli Xu1Shihao Wu1Xue Gong1Weiping Han1Yu Zhang1
Ying Li2*- 1The Second Hospital of Dalian Medical University, Dalian, China
- 2the second hospital of dalian medical university, Daliam, China
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This study demonstrates that palmitoylation-deficient CD82 (C5A/C74A/C83A mutant) exhibits reduced protein palmitoylation, increased co-localization with early endosome (EEA1) and vesicular (VPS4A) markers, and triggers mitochondrial-mediated apoptosis in MDA-MB-231 breast cancer cells, as evidenced by elevated Caspase-3, Cleaved-caspase-3, and Cytochrome C levels.Strikingly, the CD82 mutation synergistically enhanced the cytotoxic effects of both the tyrosine kinase inhibitor gefitinib and the chemotherapeutic agent doxorubicin, as quantified by TUNEL and Annexin V/PI assays.These findings reveal a previously unrecognized role of CD82 palmitoylation in modulating drug sensitivity, where its disruption potentiates chemotherapy-induced apoptosis. Our work provides a molecular rationale for targeting CD82 palmitoylation as a combinatorial strategy to overcome therapeutic resistance in triple-negative breast cancer.
Keywords: CD82, palmitoylation, Apoptosis, drug sensitivity, breast cancer
Received: 05 Sep 2025; Accepted: 17 Nov 2025.
Copyright: © 2025 Li, Yu, Chen, Zhang, Zhang, Yao, Xu, Wu, Gong, Han, Zhang and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Ying Li, liyingketizu@163.com
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