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cs.AI, q-bio.NC updates on arXiv.org
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Reflect-Guard: Enhancing LLM Safeguards against Adversarial Prompts via Logical Self-Reflection
arXiv:2605.24834v1 Announce Type: cross Abstract: Large language model (LLM) safety classifiers such as Llama Guard are effective at detecting overtly harmful prompts but remain vulnerable to adversarial jailbreak attacks that disguise malicious intent through role-play scenarios, fictional framing, and indirect requests. We present Reflect-Guard, a method that augments LLM-based safety classifiers with chain-of-thought self-reflection capabilities through parameter-efficient fine-tuning. Our a
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cs.AI, q-bio.NC updates on arXiv.org
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MemSkill: Learning and Evolving Memory Skills for Self-Evolving Agents
arXiv:2602.02474v2 Announce Type: replace-cross Abstract: Most Large Language Model (LLM) agent memory systems rely on a small set of static, hand-designed operations for extracting memory. These fixed procedures hard-code human priors about what to store and how to revise memory, making them rigid under diverse interaction patterns and inefficient on long histories. To this end, we present \textbf{MemSkill}, which reframes these operations as learnable and evolvable memory skills, structured a
MemSkill: Learning and Evolving Memory Skills for Self-Evolving Agents
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Omics in Hepatocellular
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Stromal ACTA2 Counteracts TCDD-Induced Hepatocarcinogenesis via Suppression of the PI3K-AKT-mTOR Pathway
J Hepatocell Carcinoma. 2026 May 10;13:586916. doi: 10.2147/JHC.S586916. eCollection 2026.ABSTRACTPURPOSE: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental pollutant that promotes hepatocellular carcinoma (HCC) through non-genotoxic mechanisms. However, stromal regulatory factors that counteract its tumor-promoting effects remain poorly defined. This study aimed to elucidate the role of actin alpha-2 (ACTA2) in TCDD-associated hepatocarcinogenesis.METHODS: An integrative
Stromal ACTA2 Counteracts TCDD-Induced Hepatocarcinogenesis via Suppression of the PI3K-AKT-mTOR Pathway
J Hepatocell Carcinoma. 2026 May 10;13:586916. doi: 10.2147/JHC.S586916. eCollection 2026.
ABSTRACT
PURPOSE: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental pollutant that promotes hepatocellular carcinoma (HCC) through non-genotoxic mechanisms. However, stromal regulatory factors that counteract its tumor-promoting effects remain poorly defined. This study aimed to elucidate the role of actin alpha-2 (ACTA2) in TCDD-associated hepatocarcinogenesis.
METHODS: An integrative strategy combining network toxicology, Mendelian randomization, multi-omics and single-cell analyses, molecular docking and molecular dynamics simulations, along with in vitro experiments, was employed to investigate the functional role of ACTA2.
RESULTS: ACTA2 was identified as a stromal-associated factor linked to reduced HCC risk and improved patient survival. Single-cell and multi-omics analyses revealed that ACTA2 is predominantly expressed in hepatic stellate cells and fibroblast-like populations, reflecting tumor microenvironment composition rather than tumor cell-intrinsic expression. Functional enrichment analyses indicated that ACTA2 is associated with extracellular matrix remodeling and PI3K-AKT signaling. Molecular simulations demonstrated stable binding of TCDD to ACTA2 (ΞG_bind β -7.05 kcal/mol), suggesting potential structural perturbation. In vitro experiments showed that TCDD downregulated ACTA2 expression, promoted proliferation of LX-2 and cancer-associated fibroblasts (CAFs), and activated PI3K-AKT-mTOR signaling, whereas ACTA2 overexpression attenuated these effects.
CONCLUSION: ACTA2 acts as a context-dependent stromal regulator that modulates PI3K-AKT-mTOR signaling in TCDD-induced hepatocarcinogenesis. These findings highlight the importance of stromal remodeling in environmental carcinogenesis and suggest ACTA2 as a potential biomarker and therapeutic target in dioxin-associated HCC.
PMID:42148320 | PMC:PMC13175077 | DOI:10.2147/JHC.S586916