Abstract：
UNASSIGNED: Dysregulated expression of Forkhead Box N2 (FOXN2) has been detected in various cancer types. However, the underlying mechanisms by which FOXN2 contributes to the onset and progression of gastric cancer (GC) remain largely unexplored. This study aimed to elucidate the potential role of FOXN2 within GC, its downstream molecular mechanisms, and its feasibility as a novel serum biomarker for GC.
UNASSIGNED: Tissue samples from GC patients and corresponding non-cancerous tissues were collected. Peripheral blood samples were obtained from GC patients and healthy controls. The expression of FOXN2 was determined using quantitative real-time PCR, western blotting, and immunohistochemistry. The expression of FOXN2 in GC cells was modulated by transfection with small interfering RNA (siRNA) or the pcDNA 3.1 expression vector. Cell proliferation was assessed using the Cell Counting Kit-8 and 5-ethynyl-2\'-deoxyuridine incorporation assays. The migratory and invasive capacities of cells were evaluated by Transwell assays, apoptosis rates were measured by flow cytometry, and the expression of proliferative, apoptotic, and epithelial-mesenchymal transition (EMT) markers were assessed by western blot analysis.
UNASSIGNED: FOXN2 was found to be overexpressed in the serum, tissues, and cells of GC, correlating with distant metastasis and TNM staging. FOXN2 demonstrated diagnostic value in differentiating GC patients from healthy individuals, with higher levels of FOXN2 being indicative of poorer survival rates. Silencing FOXN2 in vitro inhibited the proliferation, invasion, migration, and EMT of GC cells, while promoting apoptosis. FOXN2 was shown to regulate the transforming growth factor-beta (TGFβ) receptor signaling pathway in GC cells via its interaction with Partitioning Defective 6 Homolog Alpha (PARD6A).
UNASSIGNED: In summary, our data suggest that FOXN2 acts as an oncogenic factor in GC, modulating the TGFβ pathway by binding to PARD6A, thereby influencing gastric carcinogenesis. This study underscores the functional significance of FOXN2 as a potential serum biomarker and therapeutic target in GC.
UNASSIGNED: Tissue samples from GC patients and corresponding non-cancerous tissues were collected. Peripheral blood samples were obtained from GC patients and healthy controls. The expression of FOXN2 was determined using quantitative real-time PCR, western blotting, and immunohistochemistry. The expression of FOXN2 in GC cells was modulated by transfection with small interfering RNA (siRNA) or the pcDNA 3.1 expression vector. Cell proliferation was assessed using the Cell Counting Kit-8 and 5-ethynyl-2\'-deoxyuridine incorporation assays. The migratory and invasive capacities of cells were evaluated by Transwell assays, apoptosis rates were measured by flow cytometry, and the expression of proliferative, apoptotic, and epithelial-mesenchymal transition (EMT) markers were assessed by western blot analysis.
UNASSIGNED: FOXN2 was found to be overexpressed in the serum, tissues, and cells of GC, correlating with distant metastasis and TNM staging. FOXN2 demonstrated diagnostic value in differentiating GC patients from healthy individuals, with higher levels of FOXN2 being indicative of poorer survival rates. Silencing FOXN2 in vitro inhibited the proliferation, invasion, migration, and EMT of GC cells, while promoting apoptosis. FOXN2 was shown to regulate the transforming growth factor-beta (TGFβ) receptor signaling pathway in GC cells via its interaction with Partitioning Defective 6 Homolog Alpha (PARD6A).
UNASSIGNED: In summary, our data suggest that FOXN2 acts as an oncogenic factor in GC, modulating the TGFβ pathway by binding to PARD6A, thereby influencing gastric carcinogenesis. This study underscores the functional significance of FOXN2 as a potential serum biomarker and therapeutic target in GC.
摘要：
■已在各种癌症类型中检测到叉头盒N2（FOXN2）的表达失调。然而,FOXN2促进胃癌(GC)发病和进展的潜在机制仍未被研究.本研究旨在阐明FOXN2在GC中的潜在作用，其下游分子机制，及其作为GC新型血清生物标志物的可行性。
■收集来自GC患者的组织样品和相应的非癌组织。从GC患者和健康对照获得外周血样品。使用定量实时PCR测定FOXN2的表达，西方印迹,和免疫组织化学。通过用小干扰RNA(siRNA)或pcDNA3.1表达载体转染来调节FOXN2在GC细胞中的表达。使用细胞计数试剂盒-8和5-乙炔基-2'-脱氧尿苷掺入测定法评估细胞增殖。通过Transwell分析评估细胞的迁移和侵袭能力，通过流式细胞术测量细胞凋亡率，和增殖的表达，凋亡，通过蛋白质印迹分析评估上皮-间质转化（EMT）标志物。
■发现FOXN2在血清中过度表达，组织，和GC的细胞，与远处转移和TNM分期相关。FOXN2在区分GC患者和健康个体方面具有诊断价值，较高的FOXN2水平表明存活率较差。体外沉默FOXN2抑制细胞增殖,入侵,迁移,和GC细胞的EMT，同时促进细胞凋亡。显示FOXN2通过其与PartitioningDefective6同系物α（PARD6A）的相互作用来调节GC细胞中的转化生长因子-β（TGFβ）受体信号通路。
■总之，我们的数据表明FOXN2在GC中充当致癌因子，通过与PARD6A结合调节TGFβ途径，从而影响胃癌的发生。这项研究强调了FOXN2作为GC中潜在的血清生物标志物和治疗靶标的功能意义。
■收集来自GC患者的组织样品和相应的非癌组织。从GC患者和健康对照获得外周血样品。使用定量实时PCR测定FOXN2的表达，西方印迹,和免疫组织化学。通过用小干扰RNA(siRNA)或pcDNA3.1表达载体转染来调节FOXN2在GC细胞中的表达。使用细胞计数试剂盒-8和5-乙炔基-2'-脱氧尿苷掺入测定法评估细胞增殖。通过Transwell分析评估细胞的迁移和侵袭能力，通过流式细胞术测量细胞凋亡率，和增殖的表达，凋亡，通过蛋白质印迹分析评估上皮-间质转化（EMT）标志物。
■发现FOXN2在血清中过度表达，组织，和GC的细胞，与远处转移和TNM分期相关。FOXN2在区分GC患者和健康个体方面具有诊断价值，较高的FOXN2水平表明存活率较差。体外沉默FOXN2抑制细胞增殖,入侵,迁移,和GC细胞的EMT，同时促进细胞凋亡。显示FOXN2通过其与PartitioningDefective6同系物α（PARD6A）的相互作用来调节GC细胞中的转化生长因子-β（TGFβ）受体信号通路。
■总之，我们的数据表明FOXN2在GC中充当致癌因子，通过与PARD6A结合调节TGFβ途径，从而影响胃癌的发生。这项研究强调了FOXN2作为GC中潜在的血清生物标志物和治疗靶标的功能意义。
