High-speed atomic force microscopy and solution biophysics reveal a striking spectrum of molecular behavior in glycan-building enzymes, from a rigid dimer to flexible, reversible assemblies. POMGNT2 maintained a rigid dimeric architecture, while LARGE1 showed flexible interdomain motion and concentration-dependent assembly. K4CP displayed dramatic opening and closing movements between its domains. The findings uncover diverse dynamic architectures and suggest how structural rigidity and flexibility contribute to distinct roles in glycan synthesis.

A comprehensive review published in iMetaMed reveals that cysteine peptidases, particularly cathepsins B, S, L, and X, serve as critical regulators of antigen-presenting cell function and antitumor immunity. The study systematically elucidates how these enzymes govern antigen processing, MHC loading, cross-presentation, and immune signaling, while their dysregulation drives tumor immune evasion through excessive antigen degradation and checkpoint modulation. The authors propose that targeted modulation of cysteine peptidase activity represents a promising strategy to overcome immunotherapy resistance.

Researchers have mapped 895,475 individual cells to uncover shared features of bone metastases across 10 cancer types. The study reveals cancer growth programs alongside widespread changes in immune and supporting cells. Laboratory experiments highlight CXCL12–CXCR4 signaling as a potential link between immune-cell retention in surrounding tissue and cancer-cell migration, providing a basis for further therapeutic research.

Tumorigenesis involves transcriptomic alterations at both gene and isoform levels. While short-read RNA-seq cann’t fully resolve isoform-level changes, long-read RNA sequencing (lrRNA-seq) overcomes this limitation. In this study, we analyzed 144 paired tumor-normal transcriptomes across ten organs using lrRNA-seq. Our pan-cancer analysis revealed convergent gene expression associated with oncogenic dedifferentiation, contrasting with variable, organ-specific isoform-level alterations. Isoform-level changes, including aberrant fusion transcripts and disrupted isoform composition, were widespread and partially linked to altered splicing factor expression. Notably, many genes showed significant isoform alterations without corresponding gene expression differences. Integrating gene and isoform-level data, we developed a pan-cancer scoring framework to identify candidate prognostic correlates and potential therapeutic targets for further validation. This framework uncovered multiple underappreciated pan-cancer susceptibility genes, such as IBSP and FANCL, whose dysregulation occurs predominantly at the isoform level. Our findings advance understanding of tumor transcriptomics and provide a resource for future biomarker and therapeutic development.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the intestine. In recent years, it has been unveiled that N6-methyladenosine (also named m6A) modification, the most prevalent internal mRNA modification in mammalian cells, plays a pivotal role in the pathogenesis and development of IBD. m6A modification exerts on all four components of the intestinal barrier, including the intestinal mechanical barrier, intestinal chemical barrier, intestinal immunological barrier, and intestinal biological barrier. This paper reviews previous studies that focused on the role of m6A modification in IBD, aiming to elucidate the epigenetic mechanisms underlying IBD pathogenesis and progression, and offering novel perspectives for IBD diagnosis, treatment and prognosis prediction.

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