肺腺癌放疗过程中癌细胞不可避免地会发展出放射抗性，然而相关机制尚未完全阐明。在本研究中，我们发现肺腺癌组织中FIBP蛋白的表达上调，并与不良的总体生存率相关。功能上，我们发现FIBP的缺乏抑制了体外和体内的肺腺癌进展和放疗抗性。此外，我们揭示了FIBP与STAT3的相互作用，增强其转录活性，从而诱导下游靶基因EME1的表达。重要的是，我们证明了FIBP的生物学效应在肺腺癌中部分依赖于EME1。我们的工作揭示了FIBP通过调控STAT3/EME1轴来推动肺癌的进展和放疗抗性，表明靶向FIBP可能是肺腺癌放疗的一种新型干预策略。© 作者。

Cancer cells inevitably develop radioresistance during lung adenocarcinoma radiotherapy. However, the mechanisms are incompletely clarified. In this study, we show that FIBP protein expression in lung adenocarcinoma tissues is upregulated and associated with worse overall survival. Functionally, we find that depletion of FIBP inhibits lung adenocarcinoma progression and radioresistance in vitro and in vivo. Moreover, we uncover that FIBP interacts with STAT3 to enhance its transcriptional activity, thereby inducing the expression of the downstream target gene EME1. Importantly, we demonstrate that the biological effects of FIBP are partially dependent on EME1 in lung adenocarcinoma. Our work reveals that FIBP modulates the STAT3/EME1 axis to drive lung cancer progression and radioresistance, indicating that targeting FIBP may be a novel intervention strategy for lung adenocarcinoma radiotherapy.© The author(s).