Lung cancer remains one of the most prevalent and lethal malignancies worldwide. NSCLC, which constitutes approximately 85% of cases, continues to exhibit a poor prognosis despite advancements in therapeutic interventions, underscoring the urgent necessity to elucidate its molecular mechanisms and identify novel therapeutic targets. CD36, a multifunctional transmembrane glycoprotein, is integral to lipid uptake, immune recognition, inflammatory regulation, molecular adhesion, and apoptosis. Increasing evidence implicates CD36 in the progression of various cancers. In the context of lung cancer, CD36 facilitates tumorigenesis through multiple pathways, including the remodeling of tumor cell lipid metabolism, reprogramming of tumor-associated macrophages, and modulation of immune cell functions such as those of Tregs and CD8+T cells. Additionally, CD36 is intricately linked with the function of cancer-associated fibroblasts and the remodeling of the tumor stromal microvasculature. This systematic review synthesizes the mechanisms by which CD36 contributes to NSCLC proliferation, migration, epithelial–mesenchymal transition, and modulation of the tumor microenvironment. Furthermore, we explore emerging therapeutic strategies that target CD36. Regulating CD36 expression effectively intervenes in the malignant behavior of NSCLC, underscoring its potential as a promising therapeutic target and prognostic marker.
肺癌仍是全球范围内最高发且最具致死性的恶性肿瘤之一。其中，非小细胞肺癌约占病例的85%，尽管治疗手段不断进步，其预后仍较差，这突出阐明其分子机制及寻找新治疗靶点的迫切需要。CD36作为一种多功能跨膜糖蛋白，在脂质摄取、免疫识别、炎症调节、分子黏附和细胞凋亡中发挥着关键作用。越来越多的证据表明CD36参与多种癌症的进展。在肺癌中，CD36通过多种途径促进肿瘤发生，包括重塑肿瘤细胞脂质代谢、重编程肿瘤相关巨噬细胞，以及调节调节性T细胞和CD8⁺ T细胞等免疫细胞功能。此外，CD36与癌症相关成纤维细胞的功能及肿瘤基质微血管的重塑密切相关。本系统性综述综合阐述了CD36促进非小细胞肺癌增殖、迁移、上皮-间质转化及调控肿瘤微环境的机制。同时，我们也探讨了以CD36为靶点的新兴治疗策略。调节CD36表达可有效干预非小细胞肺癌的恶性行为，彰显其作为潜在治疗靶点与预后标志物的重要价值。
肿瘤(癌症)患者之家