Exosomal transfer of macrophage-derived NEAT1 enhances DNA damage response and confers cisplatin resistance in lung adenocarcinoma via the MAD1L1/p53 axis.

Yi Yang, Min Meng, Yi Zhao, Fangyuan Yu, Harsh Patel, Zhe-Sheng Chen

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Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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6 authors.

Yi YangShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Min MengDepartment of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.

Yi ZhaoShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Fangyuan YuDepartment of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.

Harsh PatelDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, New York, USA.

Zhe-Sheng ChenDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, New York, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin (DDP) resistance remains a major therapeutic obstacle in non-small-cell lung cancer (NSCLC). Tumor-associated macrophages (TAMs) are known to promote chemoresistance via exosomal signals, but whether exosomal long non-coding RNA NEAT1 contributes to this process is unclear. In this study, we found that exosomes derived from DDP-treated macrophages were enriched with NEAT1 and delivered it to A549 cells. This transfer enhanced the DNA damage response, promoted cell-cycle progression, and reduced DDP-induced apoptosis. Through RNA-sequencing and luciferase reporter assays, we identified MAD1L1 as a key downstream target of NEAT1. NEAT1 was enriched at the MAD1L1 promoter, upregulated its expression, and subsequently suppressed the p53/p21/Bax axis, thereby fostering a chemoresistant phenotype.

Indexed as

Adenocarcinoma of LungCell Cycle ProteinsCisplatinDNA DamageExosomesLung NeoplasmsMacrophagesNuclear ProteinsRNA, Long NoncodingTumor Suppressor Protein p53A549 CellsAnimalsAntineoplastic AgentsApoptosisCell Line, TumorDrug Resistance, NeoplasmAntineoplastic AgentsCell Cycle ProteinsCisplatinNEAT1 long non-coding RNA, humanNuclear ProteinsRNA, Long NoncodingTumor Suppressor Protein p53apoptosischemotherapy resistanceDNA damage repairexosomesmacrophagesNEAT1

Identifiers

PMID42003906

DOI10.7150/ijbs.128214

PMCPMC13086090

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.