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Tumor-associated Macrophage GnT-V Enhances Sensitivity to Antitumor Immunotherapy through Branched N-Glycosylation to Promote M1 Polarization

ABSTRACT: Tumor tissues with differential sensitivity to immunotherapy were sequenced using The DNBelab C4 /DNBelab TaiM4 Series Single-Cell Library Prep Set (MGI) was used for sequencing and sequenced on the DNBSEQ-T7 sequencer with pair-end sequencing. Immunotherapy based on immune checkpoint inhibitors (ICIs) has become one of the most successful clinical treatment strategies and has marked a milestone in the field of cancer therapy. Regrettably, the complex immunosuppressive network within the tumor microenvironment (TME), characterized by imbalanced immune cell subsets and suppressed immune cell function, represents a major cause of ICI treatment failure. This study, through single-cell analysis, provides mechanistic insights into TAM polarization and establishes the therapeutic feasibility of targeting this regulatory axis, thereby introducing a novel treatment strategy to benefit cancer patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE332556 | GEO | 2026/05/25

REPOSITORIES: GEO

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Project description:Background: Although TP53 gain-of-function (GOF) mutations promote cancer survival, its effect on EGFR-TKI efficacy remains unclear. We established EGFR-mutant lung cancer cell lines expressing various TP53 genotypes using CRISPR-Cas9 technology and found that TP53-GOF mutant cells develop an early resistance to EGFR-TKI osimertinib.The goal of this study is to elucidate the mechanisms underlying resistance to osimertinib treatment in TP53 GOF mutations through comprehensive gene analysis using RNA-seq with next-generation sequencing (NGS). Methods: Total RNA was isolated from PC-9 cells overexpressing TP53 R248Q mutation (PC9/p53R248Q: TP53 GOF mutation) and PC-9 cells overexpressing empty vector plasmid (PC9/p53EV: TP53 null) treated with DMSO or osimertinib for 24hours, using the RNeasy Micro Kit , in accordance with the manufacturer’s instructions. RNA samples were quantified by NanoDrop-2000 spectrophotometer, and the quality was confirmed with a 2200 TapeStation. rRNA was removed using MGI Easy rRNA Depletion Kit according to manufacturer's instructions followed by library construction using MGIEasy RNA Directional Library Prep Set (MGI). MGI DNBseq-G400 FAST was used to perform the amplicons deep sequencing following the standard operation protocol. The sequence format was 150bp pair read for all samples. All sequencing reads were trimmed low-quality bases and adapters with Trimmomatic (v.0.38) , and RNA sequencing reads were mapped to hg38 using HISAT2 software . Raw counts for each gene were estimated in each sample using RSEM version 1.3.0 and Bowtie 2. Calculation of the log fold-change (log FC) and p-value were performed using edgeR. Results: We explored the functions of specifically upregulated genes in TP53 GOF mutation after osimertinib treatment by KEGG pathway-enrichment analysis and found that the cytokine-cytokine receptor interaction was the most significantly altered pathway. Hallmark pathway analysis identified the TNF-α/NF-κB pathway was significantly enriched. Furthermore, TRRUST analysis showed enhanced activity of transcription factors especially RELA (p65) and NF-kB1. Conclusions: TP53 GOF mutaion induces osimertinib resistance by activating TNF-α/NF-κB pathway.

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Tumor-associated Macrophage GnT-V Enhances Sensitivity to Antitumor Immunotherapy through Branched N-Glycosylation to Promote M1 Polarization

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