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Abstract：
UNASSIGNED: Esophageal squamous cell carcinoma (ESCC) is a disease with a high incidence rate and high mortality worldwide. The Never in Mitosis A (NIMA) family member NIMA-related kinase 2 (NEK2) plays an important role in mitosis. However, the role of NEK2 in the pathogenesis of ESCC remains unclear.
UNASSIGNED: The expression and function of NEK2 in TCGA and GEO data sets were analyzed by bioinformatics. We verified the expression of NEK2 in ESCC tissues and cell lines by Western blotting and immunohistochemical methods and further explored the relationship between tumor stage and NEK2 expression. The differences in NEK2 expression and survival in patients with EC were verified by bioinformatics analysis. ESCC cell lines with stable knockdown of NEK2 were established by lentivirus-mediated shRNA delivery. The effects of NEK2 on ESCC cells were analyzed on the cytological level with assays including CCK-8, EdU, cell scratch, Transwell migration and invasion, colony formation, flow cytometry and apoptosis assays. Tumor growth was measured in a mouse xenograft model.
UNASSIGNED: We found that NEK2 is highly expressed in ESCC tissues and ESCC cells and that the high expression of NEK2 is associated with poor tumor healing. Knockdown of the NEK2 gene inhibits the migration, proliferation, invasion and cell cycle of ESCC cells. Biologic analysis shows that NEK2 is involved in biological processes such as progression and apoptosis of esophageal cancer, and is related to E2F.Mechanistically, NEK2 knockdown decreases the expression levels of E2F1 and IGF2. NEK2 competes with the transcription factor E2F1 to bind CDC20, resulting in decreased degradation and increased expression of E2F1. IGF2 expression is also increased, which promotes the expression of thymidylate synthase, further promoting the drug resistance of ESCC cells. NEK2 is associated with immune infiltration in esophageal cancer.
UNASSIGNED: NEK2 is highly expressed in ESCC and can promote the migration, proliferation and invasion of ESCC cells. NEK2 mediates ESCC immunotherapy.
UNASSIGNED: The expression and function of NEK2 in TCGA and GEO data sets were analyzed by bioinformatics. We verified the expression of NEK2 in ESCC tissues and cell lines by Western blotting and immunohistochemical methods and further explored the relationship between tumor stage and NEK2 expression. The differences in NEK2 expression and survival in patients with EC were verified by bioinformatics analysis. ESCC cell lines with stable knockdown of NEK2 were established by lentivirus-mediated shRNA delivery. The effects of NEK2 on ESCC cells were analyzed on the cytological level with assays including CCK-8, EdU, cell scratch, Transwell migration and invasion, colony formation, flow cytometry and apoptosis assays. Tumor growth was measured in a mouse xenograft model.
UNASSIGNED: We found that NEK2 is highly expressed in ESCC tissues and ESCC cells and that the high expression of NEK2 is associated with poor tumor healing. Knockdown of the NEK2 gene inhibits the migration, proliferation, invasion and cell cycle of ESCC cells. Biologic analysis shows that NEK2 is involved in biological processes such as progression and apoptosis of esophageal cancer, and is related to E2F.Mechanistically, NEK2 knockdown decreases the expression levels of E2F1 and IGF2. NEK2 competes with the transcription factor E2F1 to bind CDC20, resulting in decreased degradation and increased expression of E2F1. IGF2 expression is also increased, which promotes the expression of thymidylate synthase, further promoting the drug resistance of ESCC cells. NEK2 is associated with immune infiltration in esophageal cancer.
UNASSIGNED: NEK2 is highly expressed in ESCC and can promote the migration, proliferation and invasion of ESCC cells. NEK2 mediates ESCC immunotherapy.
摘要：
■食管鳞状细胞癌（ESCC）是世界范围内发病率高，死亡率高的疾病。Neverin有丝分裂A(NIMA)家族成员NIMA相关激酶2(NEK2)在有丝分裂中起重要作用。然而,NEK2在ESCC发病机制中的作用尚不清楚.
■通过生物信息学分析了NEK2在TCGA和GEO数据集中的表达和功能。我们通过免疫印迹和免疫组织化学方法验证了NEK2在ESCC组织和细胞系中的表达，并进一步探讨了肿瘤分期与NEK2表达的关系。通过生物信息学分析验证了EC患者NEK2表达和生存期的差异。通过慢病毒介导的shRNA递送建立具有NEK2稳定敲低的ESCC细胞系。通过包括CCK-8，EdU，细胞划痕，Transwell迁移和入侵，菌落形成,流式细胞术和细胞凋亡测定。在小鼠异种移植模型中测量肿瘤生长。
■我们发现NEK2在ESCC组织和ESCC细胞中高表达，并且NEK2的高表达与肿瘤愈合不良有关。敲除NEK2基因抑制迁移，扩散,ESCC细胞的侵袭和细胞周期。生物学分析表明，NEK2参与了食管癌的进展和凋亡等生物学过程，与E2F有关。机械上,NEK2敲低降低E2F1和IGF2的表达水平。NEK2与转录因子E2F1竞争结合CDC20，导致E2F1的降解减少和表达增加。IGF2表达也增加，促进胸苷酸合成酶的表达，进一步促进ESCC细胞的耐药性。NEK2与食管癌的免疫浸润有关。
■NEK2在ESCC中高表达，可以促进迁移，ESCC细胞的增殖和侵袭。NEK2介导ESCC免疫疗法。
■通过生物信息学分析了NEK2在TCGA和GEO数据集中的表达和功能。我们通过免疫印迹和免疫组织化学方法验证了NEK2在ESCC组织和细胞系中的表达，并进一步探讨了肿瘤分期与NEK2表达的关系。通过生物信息学分析验证了EC患者NEK2表达和生存期的差异。通过慢病毒介导的shRNA递送建立具有NEK2稳定敲低的ESCC细胞系。通过包括CCK-8，EdU，细胞划痕，Transwell迁移和入侵，菌落形成,流式细胞术和细胞凋亡测定。在小鼠异种移植模型中测量肿瘤生长。
■我们发现NEK2在ESCC组织和ESCC细胞中高表达，并且NEK2的高表达与肿瘤愈合不良有关。敲除NEK2基因抑制迁移，扩散,ESCC细胞的侵袭和细胞周期。生物学分析表明，NEK2参与了食管癌的进展和凋亡等生物学过程，与E2F有关。机械上,NEK2敲低降低E2F1和IGF2的表达水平。NEK2与转录因子E2F1竞争结合CDC20，导致E2F1的降解减少和表达增加。IGF2表达也增加，促进胸苷酸合成酶的表达，进一步促进ESCC细胞的耐药性。NEK2与食管癌的免疫浸润有关。
■NEK2在ESCC中高表达，可以促进迁移，ESCC细胞的增殖和侵袭。NEK2介导ESCC免疫疗法。
