ArticleCommunications biology2025
Elevated CD36 drives lymph node metastasis of breast cancer by activating Hippo-YAP signaling-mediated anoikis resistance.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymph node metastasis (LNM) is significantly associated with distant metastasis and poor prognosis in patients with breast cancer (BC). However, the mechanism underlying LNM in BC remains unclear, limiting the development of effective anti-metastatic strategies. Given the lipid-enriched lymphatic microenvironment, we identify the fatty acid transporter cluster of differentiation 36 (CD36) via TCGA-based screening. Aberrant expression of CD36 is positively correlated with LNM and poor prognosis in clinical specimens. BC cells with high expression of CD36 confers anoikis-resistance exposed to lymph or palmitic acid treatment. Furthermore, CD36 drives LNM in both popliteal LNM and orthotopic BC mouse models through yes-associated protein (YAP)-TEADs signaling pathway. Elevated CD36 faciliates the uptake of fatty acids and induces the PPARα-CYP7A1-bile acid biosynthesis pathway, leading to the nucleus translocation and activation of YAP by suppressing the YAP phosphorylation at Ser127. Activated YAP-TEADs complexes directly bind to the BCL2 promoter to upregulate Bcl-2 expression. Collectively, our findings identify CD36 as a critical regulator of LNM in BC and reveal a CD36-PPARα-CYP7A1-YAP regulatory axis that may provide an effective therapeutic window for preventing metastasis in BC.
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