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Overexpression of BCCIP predicts an unfavorable prognosis and promotes the proliferation and migration of lung adenocarcinoma

机译:BCCIP的过度表达预测不利的预后,促进肺腺癌的增殖和迁移

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Background Lung cancer accounts for the highest rate of cancer-related diagnosis and mortality. Lung adenocarcinoma (LUAD) is the most common histopathological type. BCCIP was originally identified as a BRCA2 and CDKN1A interacting protein. In different cancers, BCCIP plays different roles. The role of BCCIP in LUAD is still unknown. Methods The expression and prognostic value of BCCIP was analyzed using public databases, including LCE, GEPIA, TCGA, and clinical specimens. Bioinformatic analysis and vitro experiments were conducted to explore the biological functions of BCCIP in LUAD. By using the GEPIA and TIMER databases, we investigated the correlations between LUAD expression and immune infiltration in LUAD. Results Compared with normal tissue, LUAD tissue had a higher expression level of BCCIP and high expression level of BCCIP was detrimental to LUAD patient survival. The suppression of BCCIP inhibited LUAD cell proliferation, migration and resulted in G1/S phase arrest in vitro. Bioinformatic analysis demonstrated that BCCIP could be associated with cell cycle, DNA repair and E2F transcription factor family. There were significant correlations between BCCIP expression and immune infiltrates, including B cell, CD4 T cell, macrophage, neutrophil and dendritic cells. Furthermore, BCCIP expression showed strong correlations with diverse immune marker sets in LUAD, such as B cell, macrophage and DC. Conclusions Overexpression of BCCIP predicts an unfavorable prognosis and promotes the proliferation and migration of lung adenocarcinoma cells. BCCIP is correlated with immune infiltration in LUAD. Suppression of BCCIP may be a potential approach in the prevention and treatment of LUAD.
机译:背景肺癌占癌症相关诊断和死亡率的最高率。肺腺癌(路障)是最常见的组织病理学类型。 BCCIP最初被识别为BRCA2和CDKN1A相互作用蛋白质。在不同的癌症中,BCCIP发挥着不同的角色。 BCCIP在路德的角色仍然不为人知。方法使用公共数据库分析BCCIP的表达和预后价值,包括LCE,GEPIA,TCGA和临床标本。进行生物信息分析和体外实验,以探讨残桥中BCCIP的生物学功能。通过使用GEPIA和TIMER数据库,我们研究了路德拉德表达与免疫浸润之间的相关性。结果与正常组织相比,路障组织具有更高的表达水平的BCCIP和高表达水平的BCCIP对管道患者存活是有害的。 BCCIP的抑制抑制了水分细胞增殖,迁移并导致体外G1 / S期捕获。生物信息分析证明BCCIP可以与细胞周期,DNA修复和E2F转录因子家族相关。 BCCIP表达和免疫渗透之间存在显着的相关性,包括B细胞,CD4 T细胞,巨噬细胞,中性粒细胞和树突细胞。此外,BCCIP表达表达与管道中的不同免疫标记组的强烈相关,例如B细胞,巨噬细胞和DC。结论BCCIP的过度表达预测不利的预后,促进肺腺癌细胞的增殖和迁移。 BCCIP与拉德的免疫浸润相关。 BCCIP的抑制可能是预防和治疗管道的潜在方法。

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