Hohhot First Hospital

Lactylation, a lactate-derived post-translational modification, emerges as a master metabolic regulator of resistance to regulated cell death (RCD) across pathologies including cancer, inflammatory disorders, and degenerative diseases. By dynamically modifying histones and non-histone proteins via lactyltransferases and delactylases, lactylation orchestrates convergent molecular pathways that suppress ferroptosis, cuproptosis, and apoptosis. This review synthesizes current understanding of lactylation as a central regulator of RCD resistance in diseases, especially in cancers. We dissect the molecular machinery through which lactylation subverts ferroptosis, cuproptosis, and apoptosis; evaluate its pathophysiological implications in diverse pathologies; and discuss emerging therapeutic strategies to disrupt lactylation-mediated cell death evasion. This metabolic-epigenetic crosstalk establishes a robust shield against RCD in disease microenvironments, promoting therapeutic resistance and pathological resilience. Targeting lactylation regulators (writers/erasers) or combining lactate modulation with RCD inducers represents a promising strategy to overcome treatment-refractory conditions in cancers.

Gastroscopy remains the cornerstone for the diagnosis and therapeutic management of upper-gastrointestinal disorders and constitutes the principal modality for detecting gastric cancer and its premalignant lesions. Early detection is pivotal to improving survival. Intragastric foam and mucus consistently impair endoscopic visualisation, constituting a primary source of missed or delayed diagnosis of early gastric cancer and other mucosal lesions and thereby reducing the detection rate of clinically significant pathology. Residual bubbles and viscous secretions adhering to the gastric surface are the principal optical barriers encountered during routine gastroscopy. Adequate mucosal preparation that effectively eliminates these contaminants is therefore essential for maximising lesion detection. The combined administration of dimethicone powder and Pronase Granules has been shown to exert potent defoaming and mucolytic activity and is explicitly recommended in recent Chinese guidelines for digestive endoscopy as the preferred pre-procedural regimen for optimising gastric surface cleanliness. An unobstructed endoscopic view is therefore mandatory, particularly for the recognition of early gastric cancer. Accumulating evidence indicates that the combined administration of dimethicone powder and Pronase Granules, augmented by sequential postural manoeuvres, is emerging as a standard pre-treatment protocol for optimising gastric mucosal cleanliness. Systematic postural manoeuvres enable the dimethicone–pronase mixture to coat the entire gastric cavity uniformly, thereby enhancing mucosal cleanliness, shortening procedure time, and increasing the detection rate of early gastric cancer.

Background: Bioinformatics identified HNSC diagnostic/prognostic lncRNAs; GSEC was selected for HNSC/OSCC validation.Methods: HNSC transcriptomic/clinical data from TCGA identified differentially expressed lncRNAs. Univariate Cox regression found prognostic lncRNAs. The top 30 lncRNAs from random forest ranking intersected with Cox results selected diagnostic biomarkers. Xiantao Academic performed pan-cancer analysis of GSEC. UALCAN and Kaplan-Meier analyzed GSEC expression, clinical correlation, prognosis, and Xiantao Academic assessed immune infiltration in HNSC. Top 200 GSEC co-expressed genes (FDR < 0,05) underwent GO/KEGG enrichment via Metascape. qRT-PCR validated GSEC expression/clinical associations in collected OSCC tissues.Results: A total of 2385 lncRNAs were differentially expressed in HNSC (1598 upregulated, 787 downregulated). Univariate Cox regression identified 1306 lncRNAs prognostic for HNSC. Intersection of the top 30 random forest-ranked lncRNAs with Cox results identified LINC02156, AL353807.5, and GSEC (ST3GAL4-AS1) as diagnostic biomarkers. GSEC was significantly upregulated in HNSC. Its expression correlated with pathological stage, clinical grade, and immune infiltration, but not with age/gender. High GSEC expression predicted poor prognosis. Enrichment of the top 200 co-expressed genes (FDR < 0,05) linked to GO terms (e.g., GO:0005788) and KEGG pathways (e.g., hsa00532). qRT-PCR confirmed GSEC overexpression in OSCC, correlating with T stage and lymph node metastasis, but not with age, sex, or differentiation grade.Conclusion: GSEC is significantly upregulated in HNSC, linked to diagnosis, prognosis, immune infiltration (validated in OSCC), specifically correlating with T stage and lymph node metastasis, indicating its pro-oncogenic role and potential as a therapeutic target, warranting further study.