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Mastering Negation: Boosting Grounding Models via Grouped Opposition-Based Learning
Hierarchical Dual-Change Collaborative Learning for UAV Scene Change Captioning
SAW: Toward a Surgical Action World Model via Controllable and Scalable Video Generation
Geometry-Guided Camera Motion Understanding in VideoLLMs
Multi-Agent Guided Policy Optimization
XSkill: Continual Learning from Experience and Skills in Multimodal Agents
Guided Policy Optimization under Partial Observability
METTL16 enhances proteasome inhibitor resistance in multiple myeloma by inhibiting eIF2α-PERK interaction and promoting PSMB5 translation
Oncogene, Published online: 13 March 2026; doi:10.1038/s41388-026-03706-y
METTL16 enhances proteasome inhibitor resistance in multiple myeloma by inhibiting eIF2α-PERK interaction and promoting PSMB5 translationIntegrated multi-omics analysis reveals that MARCKS reprograms the immunosuppressive microenvironment to drive hepatocellular carcinoma progression
NPJ Precis Oncol. 2026 Mar 11. doi: 10.1038/s41698-026-01372-7. Online ahead of print.
ABSTRACT
Hepatocellular carcinoma (HCC) is one of the most lethal malignancies worldwide, and its progression is closely linked to the establishment of an immunosuppressive tumor microenvironment. Myristoylated alanine-rich C kinase substrate (MARCKS) has been implicated in tumor biology; however, its role in regulating immune interactions in HCC remains poorly defined. Here, we performed an integrated multi-omics analysis combining bulk transcriptomics, single-cell RNA sequencing, and spatial transcriptomics to systematically investigate the expression pattern and functional relevance of MARCKS in HCC. We found that MARCKS was significantly upregulated in HCC tissues and that high MARCKS expression was associated with aggressive clinicopathological features and unfavorable prognosis. Single-cell and spatial analyses revealed that MARCKS expression was enriched in myeloid cell populations within the tumor microenvironment. Functional annotation and mIF(Multiple immunofluorescence) validation demonstrated that MARCKS expression was associated with enhanced JAK/STAT3 signaling and M2-like macrophage polarization. Consistently, MARCKS silencing in HCC cell lines reduced STAT3 phosphorylation, suppressed malignant phenotypes in vitro, inhibited tumor growth in vivo, and diminished the capacity of tumor-derived conditioned media to promote macrophage M2 polarization. Together, these findings identify MARCKS as a key regulator of the immunosuppressive tumor microenvironment in HCC and highlight its potential as a therapeutic target for overcoming immune evasion.
PMID:41813922 | DOI:10.1038/s41698-026-01372-7
Assembly of helper NLR resistosome clusters upon activation of a coiled-coil NLR
Nature, Published online: 11 March 2026; doi:10.1038/s41586-026-10215-1
SUMM2, a coiled-coil NLR, promotes the assembly of higher-order resistosome clusters to initiate cell death in plants.Risk-adaptive therapy guided by dynamic ctDNA in nasopharyngeal carcinoma
Nature, Published online: 11 March 2026; doi:10.1038/s41586-026-10244-w
A clinical trial testing whether monitoring ctDNA clearance during treatment for nasopharyngeal cancer could be used to inform decisions about an individual’s subsequent therapeutic programme shows promising results.MAPK14/SLC7A11/GPX4 axis dysregulation drives podocyte ferroptosis via mediating glycerophospholipid metabolism
Cell Death Discovery, Published online: 11 March 2026; doi:10.1038/s41420-026-02990-7
MAPK14/SLC7A11/GPX4 axis dysregulation drives podocyte ferroptosis via mediating glycerophospholipid metabolism