PDF(Pubmed)
Abstract：
UNASSIGNED: As a N6-methyladenosine reader protein, Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is a critical player in tumor progression and metastasis. However, its specific function in head and neck squamous carcinoma (HNSCC) has yet to be determined. The present study aimed to determine the role of IGF2BP2 in HNSCC.
UNASSIGNED: The expression of IGF2BP2 in HNSCC was analyzed using The Cancer Genome Atlas (TCGA) dataset and detected in HNSCC tissues and cells, respectively. Gain- and loss- of function methods were employed to study the effects of IGF2BP2 on HNSCC cell proliferation and tumorigenesis in vitro and in vivo. MicroRNAs (miRNAs) regulating IGF2BP2 were predicted using online tools and confirmed experimentally.
UNASSIGNED: We showed augmented IGF2BP2 expression in HNSCC, which correlated with poor clinical outcomes. Functional studies showed that IGF2BP2 promoted HNSCC cell proliferation by facilitating cell cycle progression while inhibiting apoptosis. We further demonstrated that IGF2BP2 could enhance HNSCC cell tumorigenesis in vivo. Mechanistically, our data revealed that miR-98-5p could directly target IGF2BP2. The interplay between IGF2BP2 and miR-98-5p is essential to drive the progression of HNSCC via the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-protein kinase B (Akt) pathway signaling pathway.
UNASSIGNED: The current study revealed the oncogenic role of IGF2BP2 and provided insights into its potential mechanism in HNSCC tumorigenesis. Additionally, IGF2BP2 might represent a promising therapeutic target and serve as prognostic biomarker in patients with HNSCC.
UNASSIGNED: The expression of IGF2BP2 in HNSCC was analyzed using The Cancer Genome Atlas (TCGA) dataset and detected in HNSCC tissues and cells, respectively. Gain- and loss- of function methods were employed to study the effects of IGF2BP2 on HNSCC cell proliferation and tumorigenesis in vitro and in vivo. MicroRNAs (miRNAs) regulating IGF2BP2 were predicted using online tools and confirmed experimentally.
UNASSIGNED: We showed augmented IGF2BP2 expression in HNSCC, which correlated with poor clinical outcomes. Functional studies showed that IGF2BP2 promoted HNSCC cell proliferation by facilitating cell cycle progression while inhibiting apoptosis. We further demonstrated that IGF2BP2 could enhance HNSCC cell tumorigenesis in vivo. Mechanistically, our data revealed that miR-98-5p could directly target IGF2BP2. The interplay between IGF2BP2 and miR-98-5p is essential to drive the progression of HNSCC via the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-protein kinase B (Akt) pathway signaling pathway.
UNASSIGNED: The current study revealed the oncogenic role of IGF2BP2 and provided insights into its potential mechanism in HNSCC tumorigenesis. Additionally, IGF2BP2 might represent a promising therapeutic target and serve as prognostic biomarker in patients with HNSCC.
摘要：
■作为N6-甲基腺苷阅读蛋白，胰岛素样生长因子2mRNA结合蛋白2（IGF2BP2）是肿瘤进展和转移的关键参与者。然而,其在头颈部鳞状细胞癌（HNSCC）中的具体功能尚未确定。本研究旨在确定IGF2BP2在HNSCC中的作用。
■使用癌症基因组图谱（TCGA）数据集分析了IGF2BP2在HNSCC中的表达，并在HNSCC组织和细胞中进行了检测，分别。采用功能增益和丧失方法研究IGF2BP2对体外和体内HNSCC细胞增殖和肿瘤发生的影响。使用在线工具预测调节IGF2BP2的微RNA(miRNA)并通过实验证实。
■我们在HNSCC中显示IGF2BP2表达增强，这与不良的临床结果相关。功能研究表明IGF2BP2通过促进细胞周期进程同时抑制细胞凋亡促进HNSCC细胞增殖。我们进一步证明IGF2BP2可以在体内增强HNSCC细胞肿瘤发生。机械上,我们的数据显示miR-98-5p可以直接靶向IGF2BP2.IGF2BP2和miR-98-5p之间的相互作用对于通过磷脂酰肌醇-4,5-二磷酸3-激酶（PI3K）-蛋白激酶B（Akt）途径信号传导途径驱动HNSCC的进展至关重要。
■当前的研究揭示了IGF2BP2的致癌作用，并为其在HNSCC肿瘤发生中的潜在机制提供了见解。此外,IGF2BP2可能代表一个有希望的治疗靶标，并作为HNSCC患者的预后生物标志物。
■使用癌症基因组图谱（TCGA）数据集分析了IGF2BP2在HNSCC中的表达，并在HNSCC组织和细胞中进行了检测，分别。采用功能增益和丧失方法研究IGF2BP2对体外和体内HNSCC细胞增殖和肿瘤发生的影响。使用在线工具预测调节IGF2BP2的微RNA(miRNA)并通过实验证实。
■我们在HNSCC中显示IGF2BP2表达增强，这与不良的临床结果相关。功能研究表明IGF2BP2通过促进细胞周期进程同时抑制细胞凋亡促进HNSCC细胞增殖。我们进一步证明IGF2BP2可以在体内增强HNSCC细胞肿瘤发生。机械上,我们的数据显示miR-98-5p可以直接靶向IGF2BP2.IGF2BP2和miR-98-5p之间的相互作用对于通过磷脂酰肌醇-4,5-二磷酸3-激酶（PI3K）-蛋白激酶B（Akt）途径信号传导途径驱动HNSCC的进展至关重要。
■当前的研究揭示了IGF2BP2的致癌作用，并为其在HNSCC肿瘤发生中的潜在机制提供了见解。此外,IGF2BP2可能代表一个有希望的治疗靶标，并作为HNSCC患者的预后生物标志物。
