HERPUD1 mediates palmitic acid-induced UPR sustaining TNBC aggressiveness and is destabilized by CK2 pharmacological inhibition
8.0
来源：
Nature
关键字：
mRNA
发布时间：
2025-11-05 23:43
摘要：
HERPUD1 is identified as a critical mediator of palmitic acid-induced unfolded protein response (UPR) in triple-negative breast cancer (TNBC), promoting tumor aggressiveness. The study demonstrates that HERPUD1 silencing enhances sensitivity to doxorubicin, suggesting its potential as a therapeutic target. Additionally, CK2-mediated phosphorylation is highlighted as a key regulatory mechanism for HERPUD1 stability, linking it to obesity-related tumor progression and indicating the need for novel therapeutic strategies in TNBC.
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关键证据
HERPUD1 is overexpressed in breast cancer tissues, particularly in TNBC.
Silencing HERPUD1 enhances sensitivity to doxorubicin, indicating its role in chemoresistance.
CK2-mediated phosphorylation is identified as a key regulatory mechanism for HERPUD1 stability.
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AI评分总结
HERPUD1 is identified as a critical mediator of palmitic acid-induced unfolded protein response (UPR) in triple-negative breast cancer (TNBC), promoting tumor aggressiveness. The study demonstrates that HERPUD1 silencing enhances sensitivity to doxorubicin, suggesting its potential as a therapeutic target. Additionally, CK2-mediated phosphorylation is highlighted as a key regulatory mechanism for HERPUD1 stability, linking it to obesity-related tumor progression and indicating the need for novel therapeutic strategies in TNBC.