BMSC-derived exosomes promote oxaliplatin resistance in GC through activation of the G3BP1-YWHAZ axis. BXD restores chemosensitivity by interfering with this exosome-mediated pathway, supporting its use as a potential adjuvant strategy to overcome chemotherapy resistance.

This study provided potential therapeutic possibilities for oxaliplatin resistance, contributing to CRC treatment.

Mechanistic studies (RNA-seq, ChIP, SPR, etc.) confirmed the direct YBX1-bufalin interaction. Our work reveals YBX1/STC1-mediated glycolysis as a novel resistance mechanism and identifies bufalin as a promising therapeutic agent to overcome it.

In vivo studies demonstrated that MO@Ti40 NVs significantly impede tumor progression with markedly reduced systemic toxicity compared to free OXA. By integrating targeted chemotherapy with comprehensive immune reprogramming, this platform offers a promising therapeutic strategy for refractory malignancies like PDAC.

Furthermore, bioinformatic predictions combined with experimental validation (RT-PCR, ELISA, and drug sensitivity assays) demonstrated that high PPDPF expression fosters an immunosuppressive tumor microenvironment and confers resistance to 5-Fluorouracil and Oxaliplatin. In conclusion, this study is the first to establish PPDPF as a critical molecular driver that promotes malignant progression, orchestrates an immunosuppressive microenvironment, and mediates chemotherapy resistance in gastric cancer. Our findings position PPDPF as a potential novel prognostic biomarker and therapeutic target, providing a theoretical foundation for developing personalized treatment strategies for patients with gastric cancer.

In silico drug sensitivity analysis further suggested that high-risk patients may develop poorer sensitivity to five clinical drugs, including Cisplatin, Oxaliplatin, and Vinorelbine. The six-m7G-related-lncRNA signature represents a promising prognostic tool for EGC that may facilitate personalized risk stratification and guide clinical decision-making regarding adjuvant or immunotherapeutic strategies.

In aggressive WiDr cells carrying TP53 R273H mutation, knockout of UGCG gene using CRISPR/Cas9 editing or inhibition of GCS with Genz-161 sensitized cancer cells to oxaliplatin, irinotecan and paclitaxel. Conversely, inhibition of GCS can diminish CSCs and drug resistance via reduction in m6A modification and advance of p53-assocaited tumor suppressive function. GCS inhibition is an achievable approach for mutant cancer treatment.

In vivo experiments further confirmed that the SNHG15/miR-451a/CAV1 axis affected gastric cancer oxaliplatin resistance by regulating fatty acid β-oxidation. Implications: This study revealed that SNHG15 inhibits miR-451a to upregulate CAV1 expression, thereby regulating fatty acid β-oxidation and influencing gastric cancer oxaliplatin resistance, providing new biomarkers and potential therapeutic targets for gastric cancer oxaliplatin resistance.

Therapy significantly elevates expression of MHC-I on antigen-presenting immune cell subsets, increases the frequency of activated plasmacytoid dendritic cells and tumor-infiltrating CD8+ T cells, as well as depleted primarily immunosuppressive M2 macrophages. These results demonstrate that tumor-targeted oxaliplatin(IV)-based prodrugs carrying TLR7/8 agonists offer a potent dual-release strategy for improved immunochemotherapy, while minimizing excessive immune responses associated with systemic TLR7/8 activation.

Moreover, DHA impaired the regrowth of oxaliplatin-tolerant persister cells and enhanced oxaliplatin efficacy in sequential treatment models. Together, these findings indicate that exploiting the intrinsic oxidative vulnerability of cancer cells with DHA may represent a promising, low-toxicity strategy to enhance chemotherapy efficacy and target drug-tolerant persister cells in colorectal cancer.

The patient completed six cycles of adjuvant chemotherapy with tegafur-gimeracil-oteracil (S-1) plus oxaliplatin, and routine follow-up examinations showed no evidence of recurrence...The patient was treated with SOX chemotherapy combined with the PD-1 inhibitor tislelizumab...This case highlights the importance of vigilance for rare metastatic sites, such as the adrenal gland, in patients with advanced gastric cancer even after standardized postoperative surveillance. Systemic chemotherapy combined with immunotherapy may represent an effective treatment strategy for selected patients with metastatic gastric cancer.

Both CHGA and UCHL1-activated transcription were regulated through the Rho/ERK/NF-κB signaling pathways by histone modifications of H3K4 trimethylation. In this study, Rho/ERK/NFκB signaling-mediated CHGA and UCHL1 expression, which is regulated through histone modifications and affects OXA-resistant CRC EMT outcomes, was assessed, and its potential as an early detection biomarker and prognostic indicator was explored with clinical applications.