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Received — 15 September 2026 ⏭

When Does AI Augment Work? A Workflow-Level Framework for Human-Agent Collaboration

✇cs.AI, q-bio.NC updates on arXiv.org
By: AI Collaboration · Jiaying Wu · Caleb Ziems · Raymond Chan · Nancy F. Chen · Corlyss Chua · Gerard Chung · Jungpil Hahn · Wee Sun Lee · Zhengyuan Liu · Jamie Ng · Desmond C. Ong · Jeryl Ong · Da Ren Soon · Tianqi Song · Zhi-Xuan Tan · Sixing Tao · Emily Yang · Yajing Yang · Stella Xin Yin · Min-Yen Kan · Diyi Yang
14 September 2026 at 12:00
arXiv:2609.12482v1 Announce Type: new Abstract: We aim to characterise the value of artificial intelligence in the workplace. Current studies largely measure this value in terms of the current automation capabilities and public adoption of AI. However, such metrics ignore the greater impacts of human--agent collaboration in transforming the nature of work. To account for this, we must expand the scope of our analysis beyond atomised tasks of today, and instead focus on how AI can augment entire workflows of the future. To ground this analysis, we establish a precise definition of AI augmentation comprising six conditions, spanning durable net value, meaningful human control, accountability and recovery, and long-term human development through learning, career pathways, and job purpose. We elaborate on these conditions and apply the framework in a case study of AI-mediated social surveys. We conclude by outlining how organisations, researchers, and government leaders can use this framework to make sense of the future of work.
Received — 10 September 2026 ⏭

MCAT-mediated mitochondrial fatty acid metabolism regulates Lauren subtype divergence and suppresses gastric cancer progression through ROS/P53-dependent mitophagy and ferroptosis

✇Omics in Gastric
By: Yufei Wang · Meng Zhu · Xin Yin · Tianyi Fang · Lei Zhang · Yujuan Jiao · Hongxin Wang · Zipu Dong · Tengteng Liu · Yingwei Xue
9 September 2026 at 18:00

Cell Death Differ. 2026 Sep 8. doi: 10.1038/s41418-026-01867-7. Online ahead of print.

ABSTRACT

Gastric cancer (GC) displays marked heterogeneity under the Lauren classification, yet the metabolic determinants of subtype divergence remain unclear. Here, we identify Malonyl-CoA:ACP transacylase (MCAT), a Lauren subtype-associated gene encoding a key mitochondrial fatty acid synthesis (mtFAS) enzyme, as a subtype-specific tumor suppressor in GC. Integrative multi-omics profiling revealed that MCAT expression is enriched in intestinal-type GC and correlates with favorable prognosis. Mechanistically, MCAT overexpression drives metabolic reprogramming through mitochondrial free fatty acid overload, suppressing β-oxidation while elevating mitochondrial reactive oxygen species (ROS), which triggers P53 phosphorylation at Ser15. This event concurrently activates PINK1/Parkin-mediated mitophagy and suppresses the SLC7A11/GPX4 axis to induce ferroptosis. Genetic rescue experiments confirmed that P53-Ser15 phosphorylation is essential for both mitophagy and ferroptosis induction. Endogenous MCAT levels are sufficient to determine basal ROS/P53/mitophagy/ferroptosis axis activity, and knockdown in high-expressing cells reverses these phenotypes, supporting a physiological, threshold-dependent role. In vivo, MCAT overexpression suppresses tumor growth and enhances mitophagy and ferroptosis markers. Collectively, these findings establish MCAT as a metabolic switch that links mtFAS to ROS/P53-dependent cell death, providing a potential biomarker and therapeutic target for GC.

PMID:42711380 | DOI:10.1038/s41418-026-01867-7

MCAT-mediated mitochondrial fatty acid metabolism regulates Lauren subtype divergence and suppresses gastric cancer progression through ROS/P53-dependent mitophagy and ferroptosis

✇(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Yufei Wang · Meng Zhu · Xin Yin · Tianyi Fang · Lei Zhang · Yujuan Jiao · Hongxin Wang · Zipu Dong · Tengteng Liu · Yingwei Xue
9 September 2026 at 18:00

Cell Death Differ. 2026 Sep 8. doi: 10.1038/s41418-026-01867-7. Online ahead of print.

ABSTRACT

Gastric cancer (GC) displays marked heterogeneity under the Lauren classification, yet the metabolic determinants of subtype divergence remain unclear. Here, we identify Malonyl-CoA:ACP transacylase (MCAT), a Lauren subtype-associated gene encoding a key mitochondrial fatty acid synthesis (mtFAS) enzyme, as a subtype-specific tumor suppressor in GC. Integrative multi-omics profiling revealed that MCAT expression is enriched in intestinal-type GC and correlates with favorable prognosis. Mechanistically, MCAT overexpression drives metabolic reprogramming through mitochondrial free fatty acid overload, suppressing β-oxidation while elevating mitochondrial reactive oxygen species (ROS), which triggers P53 phosphorylation at Ser15. This event concurrently activates PINK1/Parkin-mediated mitophagy and suppresses the SLC7A11/GPX4 axis to induce ferroptosis. Genetic rescue experiments confirmed that P53-Ser15 phosphorylation is essential for both mitophagy and ferroptosis induction. Endogenous MCAT levels are sufficient to determine basal ROS/P53/mitophagy/ferroptosis axis activity, and knockdown in high-expressing cells reverses these phenotypes, supporting a physiological, threshold-dependent role. In vivo, MCAT overexpression suppresses tumor growth and enhances mitophagy and ferroptosis markers. Collectively, these findings establish MCAT as a metabolic switch that links mtFAS to ROS/P53-dependent cell death, providing a potential biomarker and therapeutic target for GC.

PMID:42711380 | DOI:10.1038/s41418-026-01867-7

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