László Loretta, Lovrics Anna, Tilajka Álmos, Takács Tamás, Buday László, Vas Virag
Institute of Molecular Life Sciences, HUN-REN Research Centre for Natural Sciences, Budapest, 1117, Hungary.
Doctoral School of Biology, Institute of Biology, ELTE Eötvös Loránd University, Budapest, 1117, Hungary.
Biotechnol Rep (Amst). 2025 Jun 23;47:e00902. doi: 10.1016/j.btre.2025.e00902. eCollection 2025 Sep.
Cancer rarely results from a single gene defect but emerges from disruptions in complex cellular networks. The Network Medicine perspective guides our investigation of cancer-driving interactions, particularly focusing on RAS signaling pathways that are key mediator for cancer development. We analyzed gene expression patterns in colon and lung cancers to identify stage-specific molecular drivers. Using computational modelling combined with patient tissue analysis, we discovered five key genes that are specifically altered in early-stage colon cancer: RAF1, PLCE1, RGL1, RIN1, and GRB7. These genes work as RAS effectors in signaling and can effectively distinguish between normal and cancerous colon tissue. Our approach combines network analysis with gene expression studies to understand how RAS signaling disruption contributes to colon cancer development. These findings suggest that targeting early-stage RAS-related changes could offer therapeutic opportunities before cancer becomes more complex and harder to treat.
癌症很少由单一基因缺陷导致，而是源于复杂细胞网络的紊乱。网络医学视角指导我们对驱动癌症的相互作用进行研究，尤其关注作为癌症发展关键介质的RAS信号通路。我们分析了结肠癌和肺癌中的基因表达模式，以识别阶段特异性分子驱动因素。通过结合计算建模和患者组织分析，我们发现了五个在早期结肠癌中发生特异性改变的关键基因：RAF1、PLCE1、RGL1、RIN1和GRB7。这些基因在信号传导中作为RAS效应器发挥作用，并且能够有效区分正常结肠组织和癌性结肠组织。我们的方法将网络分析与基因表达研究相结合，以了解RAS信号破坏如何促进结肠癌的发展。这些发现表明，针对早期与RAS相关的变化进行靶向治疗，可能在癌症变得更加复杂且更难治疗之前提供治疗机会。
