Ming Fei, Zhang DaiPing
Department of the Thoracic Surgery, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 116 Zhuodaoquan South Road, Hongshan District, Wuhan, 430070, Hubei, China.
Department of Cardiac Function, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430070, Hubei, China.
Biochem Genet. 2025 Jan 3. doi: 10.1007/s10528-024-11006-x.
Lung adenocarcinoma (LUAD) is characterized by its aggressive nature and resistance to treatment. FAM107A is a tumor suppressor gene that has been found to possess inhibitory effects in several cancers, but its role in LUAD remains unclear. This study investigated the role of FAM107A in regulating LUAD cell growth, invasion and aerobic glycolysis and also investigated the potential underlying mechanisms. Our findings revealed that FAM107A is significantly downregulated in LUAD, and its overexpression inhibited LUAD cell growth and invasion. Furthermore, FAM107A overexpression suppressed the anaerobic phase of carbohydrate metabolism in LUAD cells. Mechanistically, FAM107A regulated the CRYAB/PI3K/AKT signaling pathway, thereby inhibiting tumor progression, and similar findings were confirmed in our in vivo mouse model. In conclusion, FAM107A can suppress LUAD progression by regulating the CRYAB/PI3K/AKT pathway and aerobic glycolysis, indicating its potential as therapeutic target for LUAD.
肺腺癌（LUAD）具有侵袭性强和对治疗耐药的特点。FAM107A是一种肿瘤抑制基因，已发现在多种癌症中具有抑制作用，但其在LUAD中的作用仍不清楚。本研究调查了FAM107A在调节LUAD细胞生长、侵袭及有氧糖酵解中的作用，并探究了潜在的机制。我们的研究结果显示，FAM107A在LUAD中显著下调，其过表达抑制了LUAD细胞的生长和侵袭。此外，FAM107A过表达抑制了LUAD细胞碳水化合物代谢的无氧阶段。机制上，FAM107A调节CRYAB/PI3K/AKT信号通路，从而抑制肿瘤进展，我们的体内小鼠模型也证实了类似的结果。总之，FAM107A可通过调节CRYAB/PI3K/AKT通路和有氧糖酵解来抑制LUAD进展，表明其作为LUAD治疗靶点的潜力。
