ArticleCellular oncology (Dordrecht, Netherlands)2025
CAFs mediate carboplatin resistance in LUAD via CXCL12 secretion regulated by NF-κB activation.
Article in Cellular oncology (Dordrecht, Netherlands), 2025. 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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Who cites it
2 citing papers in PubMed.
- How optimal control of cellular cost shapes population-level tumor growth dynamics.bioRxiv : the preprint server for biology · 2026Article
- Cancer-Associated Fibroblast-Targeted Nanomedicine in Solid Tumor Therapy: From Mechanisms of Therapeutic Resistance to Precision Stromal Modulation.International journal of nanomedicine · 2026Review
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Authors and funding
18 authors.
Funding
Abstract
purposeCancer-associated fibroblasts (CAFs) are major constituents of the tumor microenvironment (TME) and have been associated with chemotherapeutic failure via different mechanisms. However, the CAFs inhibit chemotherapy mechanism in lung adenocarcinoma (LUAD) remains undetermined.
methodsFibroblasts were isolated from tumor and normal lung tissues from patients with poorly differentiated LUAD (pCAFs), moderately differentiated LUAD (mCAFs), and normal fibroblasts (NFs). Then, the influence of these fibroblasts on carboplatin's cytotoxic effects on LUAD cell lines A549 and NCI-H1299 was assessed by measuring their IC
resultsThe data revealed that pCAFs significantly inhibited apoptosis in LUAD cells and increased carboplatin IC
conclusionThis study revealed that LUAD-derived CAFs activate the NF-κB axis to secrete CXCL12, thereby weakening the carboplatin's killing effect on LUAD. Furthermore, poorly differentiated LUAD secreted more CXCL12. These findings indicate a novel strategy to enhance carboplatin's chemotherapeutic potential against LUAD.
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