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Safety in Embodied AI: A Survey of Risks, Attacks, and Defenses

arXiv:2605.02900v2 Announce Type: replace-cross Abstract: Embodied Artificial Intelligence (Embodied AI) integrates perception, cognition, planning, and interaction into agents that operate in open-world, safety-critical environments. As these systems gain autonomy and enter domains such as transportation, healthcare, and industrial or assistive robotics, ensuring their safety becomes both technically challenging and socially indispensable. Unlike digital AI systems, embodied agents must act under uncertain sensing, incomplete knowledge, and dynamic human-robot interactions, where failures can directly lead to physical harm. This survey provides a comprehensive and structured review of safety research in embodied AI, examining attacks and defenses across the full embodied pipeline, from perception and cognition to planning, action and interaction, and agentic system. We introduce a multi-level taxonomy that unifies fragmented lines of work and connects embodied-specific safety findings with broader advances in vision, language, and multimodal foundation models. Our review synthesizes insights from over 500 papers spanning adversarial, backdoor, jailbreak, and hardware-level attacks; attack detection, safe training and robust inference; and risk-aware human-agent interaction. This analysis reveals several overlooked challenges, including the fragility of multimodal perception fusion, the instability of planning under jailbreak attacks, and the trustworthiness of human-agent interaction in open-ended scenarios. By organizing the field into a coherent framework and identifying critical research gaps, this survey provides a roadmap for building embodied agents that are not only capable and autonomous but also safe, robust, and reliable in real-world deployment.

SNHG12 drives gastric cancer progression by activating the Wnt/beta-catenin-mediated serine synthesis pathway

1 May 2026 at 18:00

J Transl Med. 2026 Apr 30;24(1):638. doi: 10.1186/s12967-026-08173-3.

ABSTRACT

BACKGROUND: Metabolic reprogramming is a hallmark of gastric cancer and is essential for sustaining rapid proliferation and malignant progression. The serine synthesis pathway (SSP), a key branch of glycolysis coupled to one-carbon metabolism (OCM), plays a central role in nucleotide biosynthesis, redox homeostasis, and epigenetic regulation. Although aberrant SSP activation has been implicated in gastric cancer, its upstream regulatory mechanisms remain poorly defined. Long non-coding RNAs (lncRNAs) have emerged as critical modulators of oncogenic signaling and metabolism. This study aimed to elucidate the role of the lncRNA SNHG12 in gastric cancer progression and to determine whether it drives metabolic reprogramming through the Wnt/β-catenin-SSP axis.

METHODS: SNHG12 expression and clinical relevance were analyzed using public datasets, clinical gastric cancer specimens, and cell lines. Gain- and loss-of-function experiments were performed to assess the effects of SNHG12 on proliferation, apoptosis, migration, and invasion. Transcriptomic profiling, targeted metabolomics, and integrative multi-omics analyses were used to characterize metabolic alterations. Pharmacological inhibition of SSP (NCT503) and Wnt/β-catenin signaling (IWR-1) was applied in vitro and in vivo. A subcutaneous xenograft mouse model was used to validate tumor-promoting effects and therapeutic responses.

RESULTS: SNHG12 was significantly upregulated in gastric cancer tissues and cell lines and was associated with poor overall and progression-free survival. Functionally, SNHG12 promoted gastric cancer cell proliferation, migration, and invasion while suppressing apoptosis. Transcriptomic and targeted metabolomic analyses revealed broad metabolic alterations associated with SNHG12, including changes in serine/one-carbon metabolism, purine biosynthesis, and glutathione-related pathways. Mechanistically, SNHG12 increased Wnt/β-catenin reporter activity, promoted β-catenin nuclear accumulation, and was accompanied by increased expression of key SSP-associated enzymes, including PHGDH, PSAT1, and SHMT2. Pharmacological inhibition of SSP or Wnt/β-catenin signaling partially reversed SNHG12-induced malignant phenotypes in vitro and suppressed tumor growth in xenograft models.

CONCLUSIONS: This study identifies SNHG12 as an important regulator of metabolic reprogramming in gastric cancer. Our data support a model in which SNHG12 promotes gastric cancer cell proliferation, invasion, and migration through SSP regulation, and suggest that its effects on the SSP may be mediated, at least in part, through modulation of SSP-associated enzymes via the Wnt/β-catenin pathway. These findings support SNHG12 as a candidate biomarker and a potential therapeutic target for combined metabolic and signaling-based interventions in gastric cancer.

PMID:42063161 | PMC:PMC13151230 | DOI:10.1186/s12967-026-08173-3

Developmental organization of sensory and sympathetic ganglia

Nature, Published online: 01 April 2026; doi:10.1038/s41586-026-10313-0

Findings suggest that neural crest fate bias predominantly emerges within the neural tube, and that only a minor subset of delaminated progenitors retain multipotency to generate both sensory and sympathetic derivatives.
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