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When Only the Final Text Survives: Implicit Execution Tracing for Multi-Agent Attribution

arXiv:2603.17445v3 Announce Type: replace Abstract: When a multi-agent system produces an incorrect or harmful answer, who is accountable if execution logs and agent identifiers are unavailable? In practice, generated content is often detached from its execution environment due to privacy or system boundaries, leaving the final text as the only auditable artifact. Existing attribution methods rely on full execution traces and thus become ineffective in such metadata-deprived settings. We propose Implicit Execution Tracing (IET), a provenance-by-design framework that shifts attribution from post-hoc inference to built-in instrumentation. Instead of reconstructing hidden trajectories, IET embeds agent-specific, key-conditioned statistical signals directly into the token generation process, transforming the output text into a self-verifying execution record. At inference time, we recover a linearized execution trace from the final text via transition-aware statistical scoring. Experiments across diverse multi-agent coordination settings demonstrate that IET achieves accurate segment-level attribution and reliable transition recovery under identity removal, boundary corruption, and privacy-preserving redaction, while maintaining generation quality. These results show that embedding provenance into generation provides a practical and robust foundation for accountability in multi-agent language systems when execution metadata is unavailable.

Curcumol Induces G1 Phase Arrest in SK-Hep-1 Cells by Targeting SKP2-Mediated p27 Degradation

28 March 2026 at 18:00

Molecules. 2026 Mar 16;31(6):997. doi: 10.3390/molecules31060997.

ABSTRACT

CONTEXT: S-phase kinase-associated protein 2 (SKP2) is an oncogene and cell cycle regulator that mediates the ubiquitination of cell cycle regulators. Curcumol, a sesquiterpene natural product, has been reported to regulate SKP2-mediated ubiquitination degradation to overcome drug resistance in cancer cells. However, whether the cell cycle arrest effect of curcumol is related to SKP2's function in cancer cells and its mechanisms are still unclear.

OBJECTIVE: To investigate the role of SKP2 in curcumol-induced cell cycle arrest and its underlying mechanisms.

MATERIALS AND METHODS: Transcriptomic and proteomic analyses were used to screen the ubiquitination-related factors in curcumol treated hepatocellular carcinoma cells. Lentiviral overexpression, co-immunoprecipitation assays, ubiquitination analysis, and cell-line-derived xenograft (CDX) models were used to dissect the role and mechanisms of the identified ubiquitination-related factor in the cell cycle arrest effect of curcucmol.

RESULTS: Curcumol modulated the expression of CDK4, CDK6, Cyclin D1, p27 and SKP2. SKP2 was one candidate target of curcumol selected by multi-omics. Overexpressed SKP2 partially reversed curcumol-induced growth inhibition and G1-phase arrest. The increased expression of p27 induced by curcumol was attenuated by overexpressed SKP2. Curcumol impaired the interaction between SKP2 and p27, and led to the ubiquitination and degradation of p27. In vivo, curcumol effectively reduced tumor growth, and its antitumor effect was significantly mitigated by SKP2 overexpression.

DISCUSSION AND CONCLUSIONS: Curcumol reduced SKP2 expression, weakened the interaction between SKP2 and p27, inhibited degradation of p27, and then induced G1 phase cell-cycle arrest in SK-Hep-1 cells.

PMID:41900096 | PMC:PMC13029316 | DOI:10.3390/molecules31060997

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