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cs.AI, q-bio.NC updates on arXiv.org
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CODESKILL: Learning Self-Evolving Skills for Coding Agents
arXiv:2605.25430v1 Announce Type: new Abstract: Coding agents produce rich trajectories while solving software-engineering tasks. To enable agent self-evolution, these trajectories can be distilled into reusable procedural skills that compactly encode experience to guide future behavior. However, existing skill construction and maintenance methods often rely on fixed prompts and heuristic update rules, leaving it unclear how knowledge should be selected, abstracted, and maintained to best serve
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cs.AI, q-bio.NC updates on arXiv.org
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Weakly Supervised Camouflaged Object Detection Based on the SAM Model and Mask Guidance
arXiv:2605.25385v1 Announce Type: cross Abstract: Camouflaged object detection (COD) from a single image is a challenging task due to the high similarity between objects and their surroundings. Existing fully supervised methods require labor-intensive pixel-level annotations, making weakly supervised methods a viable compromise that balances accuracy and annotation efficiency. However, weakly supervised methods often experience performance degradation due to the use of coarse annotations. In th
Weakly Supervised Camouflaged Object Detection Based on the SAM Model and Mask Guidance
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Omics In Lung
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ANP32E drives lung adenocarcinoma progression via GSK3beta-mediated glycolytic reprogramming
Cell Death Dis. 2026 Apr 14. doi: 10.1038/s41419-026-08712-2. Online ahead of print.ABSTRACTLung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and atte
ANP32E drives lung adenocarcinoma progression via GSK3beta-mediated glycolytic reprogramming
Cell Death Dis. 2026 Apr 14. doi: 10.1038/s41419-026-08712-2. Online ahead of print.
ABSTRACT
Lung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and attenuated xenograft growth, while overexpression promoted tumorigenesis. Mechanistically, ANP32E transcriptionally upregulates histone demethylase KDM3B, reducing repressive H3K9me2 marks at the EGFR promoter to enhance EGFR transcription. This activates PI3K/AKT signaling, inducing inhibitory GSK3Ξ² phosphorylation. Combined with ANP32E-mediated GSK3Ξ² suppression, this dual inactivation liberates oncogenic glycolysis. Crucially, KDM3B silencing or EGFR inhibition (Cetuximab) abrogated ANP32E-driven phenotypes. High-throughput screening identified Penta-O-galloyl-Ξ²-D-glucose (PGG) as an ANP32E-targeting compound, with molecular dynamics confirming binding. PGG dose-dependently inhibited the ANP32E/KDM3B/EGFR axis in vitro and suppressed tumor growth in vivo. Thus, ANP32E drives LUAD progression via KDM3B/EGFR-mediated GSK3Ξ² inactivation, representing a prognostic biomarker and therapeutic target validated by PGG.
PMID:41980942 | DOI:10.1038/s41419-026-08712-2