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Abstract：
UNASSIGNED: Ovarian cancer is an aggressive malignancy with high mortality known for its considerable metastatic potential. This study aimed to explore the expression and functional role of Unc-51 like autophagy activating kinase 2 (ULK2) in the progression of ovarian cancer.
UNASSIGNED: ULK2 expression patterns in ovarian cancer tissues as well as benign tumor control samples obtained from our institution were evaluated using immunohistochemistry. Cell counting kit 8 and Transwell assays were applied to assess the effects of ULK2 overexpression on cell proliferation, migration and invasion, respectively. RNA sequencing was performed to explore potential mechanisms of action of ULK2 beyond its classical autophagy modulation.
UNASSIGNED: Our experiments showed significant downregulation of ULK2 in ovarian cancer tissues. Importantly, low expression of ULK2 was markedly correlated with decreased overall survival. In vitro functional studies further demonstrated that overexpression of ULK2 significantly suppressed tumor cell proliferation, migration, and invasion. RNA sequencing analysis revealed a potential regulatory role of ULK2 in the insulin signaling pathway through upregulation of insulin-like growth factor binding protein-3 (IGFBP3) in ovarian cancer cells.
UNASSIGNED: In summary, the collective data indicated that ULK2 acted as a tumor suppressor in ovarian cancer by upregulating the expression of IGFBP3. Our study underscores the potential utility of ULK2 as a valuable prognostic marker for ovarian cancer.
UNASSIGNED: ULK2 expression patterns in ovarian cancer tissues as well as benign tumor control samples obtained from our institution were evaluated using immunohistochemistry. Cell counting kit 8 and Transwell assays were applied to assess the effects of ULK2 overexpression on cell proliferation, migration and invasion, respectively. RNA sequencing was performed to explore potential mechanisms of action of ULK2 beyond its classical autophagy modulation.
UNASSIGNED: Our experiments showed significant downregulation of ULK2 in ovarian cancer tissues. Importantly, low expression of ULK2 was markedly correlated with decreased overall survival. In vitro functional studies further demonstrated that overexpression of ULK2 significantly suppressed tumor cell proliferation, migration, and invasion. RNA sequencing analysis revealed a potential regulatory role of ULK2 in the insulin signaling pathway through upregulation of insulin-like growth factor binding protein-3 (IGFBP3) in ovarian cancer cells.
UNASSIGNED: In summary, the collective data indicated that ULK2 acted as a tumor suppressor in ovarian cancer by upregulating the expression of IGFBP3. Our study underscores the potential utility of ULK2 as a valuable prognostic marker for ovarian cancer.
摘要：
■卵巢癌是一种侵袭性恶性肿瘤，死亡率高，以其巨大的转移潜力而闻名。本研究旨在探讨Unc-51样自噬激活激酶2(ULK2)在卵巢癌进展中的表达及功能。
■使用免疫组织化学评估了从我们机构获得的卵巢癌组织以及良性肿瘤对照样品中的ULK2表达模式。应用细胞计数试剂盒8和Transwell测定法来评估ULK2过表达对细胞增殖的影响。移民和入侵，分别。进行RNA测序以探索ULK2超出其经典自噬调节的潜在作用机制。
■我们的实验显示ULK2在卵巢癌组织中显著下调。重要的是,ULK2的低表达与总生存率降低显著相关.体外功能研究进一步证明ULK2的过表达显著抑制肿瘤细胞增殖,迁移,和入侵。RNA测序分析揭示了ULK2通过上调卵巢癌细胞中胰岛素样生长因子结合蛋白-3（IGFBP3）在胰岛素信号通路中的潜在调节作用。
■总之，这些数据表明ULK2通过上调IGFBP3的表达而在卵巢癌中发挥肿瘤抑制因子的作用。我们的研究强调了ULK2作为卵巢癌有价值的预后标志物的潜在效用。
■使用免疫组织化学评估了从我们机构获得的卵巢癌组织以及良性肿瘤对照样品中的ULK2表达模式。应用细胞计数试剂盒8和Transwell测定法来评估ULK2过表达对细胞增殖的影响。移民和入侵，分别。进行RNA测序以探索ULK2超出其经典自噬调节的潜在作用机制。
■我们的实验显示ULK2在卵巢癌组织中显著下调。重要的是,ULK2的低表达与总生存率降低显著相关.体外功能研究进一步证明ULK2的过表达显著抑制肿瘤细胞增殖,迁移,和入侵。RNA测序分析揭示了ULK2通过上调卵巢癌细胞中胰岛素样生长因子结合蛋白-3（IGFBP3）在胰岛素信号通路中的潜在调节作用。
■总之，这些数据表明ULK2通过上调IGFBP3的表达而在卵巢癌中发挥肿瘤抑制因子的作用。我们的研究强调了ULK2作为卵巢癌有价值的预后标志物的潜在效用。
