撰文丨王聪 编辑丨王多鱼 排版丨水成文 对海量组学数据进行分子全景分析，可识别细胞内的调控网络，但需要机制性阐释和实验验证。 2026 年 1 月 8 日， 华中科技大学 薛宇 / 彭迪 团队在 Nature 子刊 Nature Biomedical Engineering 上发表了题为： A deep learning and large language hybrid workflow for omics interpretation 的研究论文。 该研究结合深度学习 （ Deep Learning ） 与大语言模型 （ Large Language Model ） 推理能力，开发了一个名为 LyMOI 的混合组学解读工作流，利用 LyMOI，研究团队 拓展了对自噬调控因子的认知，并发现新型抗癌疗法。 在这项最新研究中，研究团队结合深度学习 （ Deep Learning ） 与大语言模型 （ Large Language Model ） 推理能力，开发了名为 LyMOI 的混合组学解读工 作流。 该工作流整合 GPT-3.5 进行生物知识推理，并采用基于图卷积网络 （ graph convolution ...

Core Insights - Lung cancer is the most prevalent cancer globally, with 2.48 million new cases and 1.8 million deaths annually, primarily due to non-small cell lung cancer (NSCLC) which accounts for over 85% of cases [2] - The recent study published by a team from Sun Yat-sen University identifies LIC1 as a new therapeutic target for NSCLC and highlights the potential of DAA as an autophagy-inducing agent for treatment [3][7] Group 1: Research Findings - The research isolated a small molecule, DAA, from endophytic fungi of Euphorbiaceae plants, which effectively induces autophagic cell death in NSCLC cells [3][5] - DAA shows significant anti-tumor efficacy in NSCLC and enhances sensitivity to anti-PD-1 immunotherapy while exhibiting low toxicity to normal lung fibroblasts [5] - LIC1 was identified as the direct target of DAA, which is overexpressed in NSCLC tumors and associated with poor prognosis [5] Group 2: Mechanism of Action - DAA disrupts the interaction between LIC1 and the stress response effector RuvBL1, enhancing the integrated stress response mediated by the GCN2-eIF2α-ATF4 signaling axis, ultimately promoting autophagic cell death [5]

Core Viewpoint - The research reveals the critical role of endocytosis in cysteine-deprivation-induced ferroptosis, challenging previous understandings of lysosomal inhibitor mechanisms and suggesting different execution pathways for ferroptosis [3][7]. Group 1: Key Findings - Lysosomal inhibitors can independently suppress cysteine-deprivation-induced (CDI) ferroptosis, regardless of autophagy [5]. - Endocytosis is essential for CDI ferroptosis but is not required for ferroptosis induced by GPX4 depletion [5]. - Endocytic defects reduce intracellular iron levels and prevent CDI ferroptosis [5]. Group 2: Mechanisms and Implications - Transferrin's clathrin-mediated endocytosis (CME) is crucial for driving CDI ferroptosis [4][5]. - Inhibition of lysosomal proteolytic activity does not prevent ferroptosis, while disrupting endosomal acidification and removing endocytic protein AP2M1 can block ferroptosis [4]. - Supplementing iron through ammonium iron citrate, independent of endocytosis, can restore CDI ferroptosis in cells with endocytic defects [4].