Abstract：
BACKGROUND: Lung adenocarcinoma (LUAD) is a leading cause of tumor-associated mortality, and it is needed to find new target to combat this disease. Guanine nucleotide-binding -protein-like 3 (GNL3) mediates cell proliferation and apoptosis in several cancers, but its role in LUAD remains unclear.
OBJECTIVE: To explore the expression and function of Guanine nucleotide-binding protein-like 3 (GNL3) in lung adenocarcinoma (LUAD) and its potential mechanism in inhibiting the growth of LUAD cells.
METHODS: We evaluated the expression of GNL3 in LUAD tissues and its association with patient prognosis using databases and immunohistochemistry. Cell proliferation was assessed by CCK-8 assay as well as colony formation, while apoptosis was evaluated by FCM. The effect of GNL3 knockdown on the Wnt/β-catenin axis was investigated by Immunoblot analysis.
RESULTS: GNL3 is overexpressed in LUAD tissues and is correlated with poor prognosis. Knockdown of GNL3 significantly inhibited the growth as well as induced apoptosis in A549 as well as H1299 cells. Furthermore, we found that the inhibitory effect of GNL3 knockdown on LUAD cell growth is associated with the downregulation of the Wnt/β-catenin axis.
CONCLUSIONS: GNL3 is key in the progression of LUAD by metiating Wnt/β-catenin axis. Targeting GNL3 may represent a novel therapeutic method for LUAD treatment.
OBJECTIVE: To explore the expression and function of Guanine nucleotide-binding protein-like 3 (GNL3) in lung adenocarcinoma (LUAD) and its potential mechanism in inhibiting the growth of LUAD cells.
METHODS: We evaluated the expression of GNL3 in LUAD tissues and its association with patient prognosis using databases and immunohistochemistry. Cell proliferation was assessed by CCK-8 assay as well as colony formation, while apoptosis was evaluated by FCM. The effect of GNL3 knockdown on the Wnt/β-catenin axis was investigated by Immunoblot analysis.
RESULTS: GNL3 is overexpressed in LUAD tissues and is correlated with poor prognosis. Knockdown of GNL3 significantly inhibited the growth as well as induced apoptosis in A549 as well as H1299 cells. Furthermore, we found that the inhibitory effect of GNL3 knockdown on LUAD cell growth is associated with the downregulation of the Wnt/β-catenin axis.
CONCLUSIONS: GNL3 is key in the progression of LUAD by metiating Wnt/β-catenin axis. Targeting GNL3 may represent a novel therapeutic method for LUAD treatment.
摘要：
背景：肺腺癌（LUAD）是肿瘤相关死亡率的主要原因，需要找到新的目标来对抗这种疾病。鸟嘌呤核苷酸结合蛋白样3（GNL3）在几种癌症中介导细胞增殖和凋亡，但其在LUAD中的作用尚不清楚。
目的：探讨鸟嘌呤核苷酸结合蛋白样3(GNL3)在肺腺癌(LUAD)中的表达、作用及其抑制LUAD细胞生长的潜在机制。
方法：我们使用数据库和免疫组织化学评估了GNL3在LUAD组织中的表达及其与患者预后的关系。通过CCK-8测定评估细胞增殖以及集落形成，而凋亡通过FCM评估。通过免疫印迹分析研究了GNL3敲低对Wnt/β-连环蛋白轴的影响。
结果：GNL3在LUAD组织中过度表达，与不良预后相关。敲除GNL3显著抑制A549和H1299细胞的生长并诱导细胞凋亡。此外，我们发现GNL3敲低对LUAD细胞生长的抑制作用与Wnt/β-catenin轴的下调有关。
结论：GNL3是通过确定Wnt/β-catenin轴在LUAD进展中的关键。靶向GNL3可能代表了LUAD治疗的新型治疗方法。
目的：探讨鸟嘌呤核苷酸结合蛋白样3(GNL3)在肺腺癌(LUAD)中的表达、作用及其抑制LUAD细胞生长的潜在机制。
方法：我们使用数据库和免疫组织化学评估了GNL3在LUAD组织中的表达及其与患者预后的关系。通过CCK-8测定评估细胞增殖以及集落形成，而凋亡通过FCM评估。通过免疫印迹分析研究了GNL3敲低对Wnt/β-连环蛋白轴的影响。
结果：GNL3在LUAD组织中过度表达，与不良预后相关。敲除GNL3显著抑制A549和H1299细胞的生长并诱导细胞凋亡。此外，我们发现GNL3敲低对LUAD细胞生长的抑制作用与Wnt/β-catenin轴的下调有关。
结论：GNL3是通过确定Wnt/β-catenin轴在LUAD进展中的关键。靶向GNL3可能代表了LUAD治疗的新型治疗方法。
