EMC2 promotes triple negative breast cancer growth by protecting FDFT1 from endoplasmic reticulum associated degradation to impair ferroptosis susceptibility
8.0
来源：
Nature
关键字：
mRNA
发布时间：
2025-09-11 07:41
摘要：
EMC2 is identified as a crucial regulator of cholesterol biosynthesis in triple-negative breast cancer (TNBC), promoting tumor growth and impairing ferroptosis susceptibility. The study reveals that EMC2 interacts with HSP90 to maintain the stability of FDFT1, a key enzyme in cholesterol synthesis, thus enhancing TNBC progression. This research underscores the potential of targeting EMC2 as a therapeutic strategy for TNBC, providing insights into the molecular mechanisms underlying cholesterol metabolism in cancer.
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domain_focus
1.0
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1.0
scientific_rigor
1.5
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2.5
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1.0
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关键证据
EMC2 is highly expressed in TNBC and predicts short survival of patients.
Targeting EMC2 could be a promising novel therapeutic target for TNBC treatment.
The study provides evidence that EMC2 regulates cholesterol biosynthesis and ferroptosis resistance.
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AI评分总结
EMC2 is identified as a crucial regulator of cholesterol biosynthesis in triple-negative breast cancer (TNBC), promoting tumor growth and impairing ferroptosis susceptibility. The study reveals that EMC2 interacts with HSP90 to maintain the stability of FDFT1, a key enzyme in cholesterol synthesis, thus enhancing TNBC progression. This research underscores the potential of targeting EMC2 as a therapeutic strategy for TNBC, providing insights into the molecular mechanisms underlying cholesterol metabolism in cancer.