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題名 MYADM Activates RhoA-Mediated Amoeboid Migration to Drive Metastasis 作者 陳紹寬
Chen, Shau-Kwaun;al, et貢獻者 神科所 日期 2025-11 上傳時間 13-Nov-2025 10:59:06 (UTC+8) 摘要 Metastasis, the leading cause of cancer-related mortality, remains the most critical challenge in cancer treatment. Cancer cells can adopt amoeboid migration to facilitate metastasis, highlighting the need to elucidate the molecular pathways regulating the amoeboid migration phenotype. In this study, we identified that MYADM, a transmembrane protein expressed during myeloid cell maturation, enabled cancer cells to acquire amoeboid migration plasticity, promoting metastasis and contributing to poor patient outcomes. Cancer cells exploited MYADM-mediated adhesion and migration to mimic leukocyte trafficking. By interacting with RhoGDI, MYADM activated RhoA-mediated leukocyte trafficking–associated gene enrichment, invasiveness, membrane blebbing, and anoikis resistance. MYADM modulated chromatin accessibility–regulatory genes, influencing intermediate filament cytoskeleton dynamics of cancer cells and tumor tissues. MYADM loss in cancer cells triggered chromatin accessibility–driven death signaling, blocking metastasis, which was not observed in monocytes. These findings position MYADM as a potential therapeutic target to disrupt metastasis, offering avenues for clinical intervention. 關聯 Cancer Research, Vol.85, No.21, pp.4099-4121 資料類型 article DOI https://doi.org/10.1158/0008-5472.CAN-25-0006 dc.contributor 神科所 dc.creator (作者) 陳紹寬 dc.creator (作者) Chen, Shau-Kwaun;al, et dc.date (日期) 2025-11 dc.date.accessioned 13-Nov-2025 10:59:06 (UTC+8) - dc.date.available 13-Nov-2025 10:59:06 (UTC+8) - dc.date.issued (上傳時間) 13-Nov-2025 10:59:06 (UTC+8) - dc.identifier.uri (URI) https://nccur.lib.nccu.edu.tw/handle/140.119/160162 - dc.description.abstract (摘要) Metastasis, the leading cause of cancer-related mortality, remains the most critical challenge in cancer treatment. Cancer cells can adopt amoeboid migration to facilitate metastasis, highlighting the need to elucidate the molecular pathways regulating the amoeboid migration phenotype. In this study, we identified that MYADM, a transmembrane protein expressed during myeloid cell maturation, enabled cancer cells to acquire amoeboid migration plasticity, promoting metastasis and contributing to poor patient outcomes. Cancer cells exploited MYADM-mediated adhesion and migration to mimic leukocyte trafficking. By interacting with RhoGDI, MYADM activated RhoA-mediated leukocyte trafficking–associated gene enrichment, invasiveness, membrane blebbing, and anoikis resistance. MYADM modulated chromatin accessibility–regulatory genes, influencing intermediate filament cytoskeleton dynamics of cancer cells and tumor tissues. MYADM loss in cancer cells triggered chromatin accessibility–driven death signaling, blocking metastasis, which was not observed in monocytes. These findings position MYADM as a potential therapeutic target to disrupt metastasis, offering avenues for clinical intervention. dc.format.extent 109 bytes - dc.format.mimetype text/html - dc.relation (關聯) Cancer Research, Vol.85, No.21, pp.4099-4121 dc.title (題名) MYADM Activates RhoA-Mediated Amoeboid Migration to Drive Metastasis dc.type (資料類型) article dc.identifier.doi (DOI) 10.1158/0008-5472.CAN-25-0006 dc.doi.uri (DOI) https://doi.org/10.1158/0008-5472.CAN-25-0006
