ArticleMedComm2026
Active Macropinocytosis, Lipid Catabolism, and Exhausting Immune Microenvironment of Ascites Tumor Cells Are Involved in Resistance to Platinum-Based Therapy in Patients With High-Grade Serous Ovarian Cancer.
Article in MedComm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
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Authors and funding
13 authors.
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Abstract
Platinum resistance remains a clinical challenge in ovarian cancer. Ascites represents an important mediator and a unique tumor microenvironment (TME) for invasion and metastasis. This study performed high-resolution mass spectrometry (MS) on pre-chemotherapy ascites cells from ovarian cancer patients. Integrating proteomic profiling, clinical data, and single-cell analysis revealed that platinum-resistant ascites displayed a distinct microenvironmental: the macropinocytosis-related protein Src homology 3 domain-containing YSC84-like 1 (SH3YL1) was upregulated, whereas the immune-activation marker CD44 was downregulated in resistant cases. Single-cell analyses and pathway enrichment indicated immune exhaustion in resistant ascites, alongside enhanced macropinocytosis and lipid catabolism in tumor cells. Clinical data also showed that resistant ascites are lipid-rich, with immunofluorescence plus flow cytometry confirming its association with immune exhaustion. Cellular experiments confirmed that SH3YL1-mediated macropinocytosis promoted lipid uptake, and its inhibition partially restored cisplatin sensitivity. A combined model of immune exhaustion, macropinocytosis, and lipid catabolism suggests these ascites-associated features could somewhat predict the platinum sensitivity in ovarian cancer tissues. We therefore propose the hypothesis that, in a lipid-rich ascites microenvironment, immune exhaustion occurs while tumor cells activate macropinocytosis and lipid catabolism-forming a network of resistance mechanisms that may serve as potential predictive markers or intervention targets for platinum resistance.
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