敲低KIF15通过激活卵巢癌中多种信号通路的串扰促进细胞凋亡：生物信息学和实验分析
Knockdown of KIF15 promotes cell apoptosis by activating crosstalk of multiple pathways in ovarian cancer: bioinformatic and experimental analysis.
作者信息
Sun Xinwei, Chen Mengyue, Liao Bin, Liang Zhiqing
机构信息
Department of Gynecology and Obstetrics, Southwest Hospital, Army Medical University Chongqing, China.
Department of Gynecology and Obstetrics, The First People's Hospital of Liang Jiang Area Chongqing, China.
出版信息
Int J Clin Exp Pathol. 2021 Feb 1;14(2):267-291. eCollection 2021.
BACKGROUND
Ovarian cancer (OC) is the most lethal malignancy of women. Unlimited proliferation is a fundamental feature of OC cells. The genes associated with cell proliferation may be histopathologic biomarkers and targets of anti-tumor therapeutic strategies. The present study aimed to identify proliferation-associated biomarkers with prognostic, diagnostic, and therapeutic value and reveal the underlying molecular mechanism of candidate genes involved in OC by a combination of bioinformatic and experimental methods.
RESULTS
KIF15 was upregulated in early-stage OC tissues and could predict poor prognosis of patients of Stage I and II. The knockdown of KIF15 significantly inhibited cell proliferation, tumor formation, and growth as well as promoting apoptosis of OC cells. A combination of experimental and bioinformatic analyses revealed KIF15 knockdown promoted cell apoptosis by activating crosstalk of multiple pathways in OC.
CONCLUSION
KIF15, an early-stage prognostic gene, was identified as a candidate histopathologic biomarker and therapeutic target of OC.
背景
卵巢癌（OC）是女性最致命的恶性肿瘤。无限增殖是OC细胞的一个基本特征。与细胞增殖相关的基因可能是组织病理学生物标志物和抗肿瘤治疗策略的靶点。本研究旨在通过生物信息学和实验方法相结合，鉴定具有预后、诊断和治疗价值的增殖相关生物标志物，并揭示OC中候选基因的潜在分子机制。
结果
KIF15在早期OC组织中上调，可预测Ⅰ期和Ⅱ期患者的不良预后。敲低KIF15可显著抑制OC细胞的增殖、肿瘤形成和生长，并促进其凋亡。实验分析和生物信息学分析相结合表明，敲低KIF15通过激活OC中多种途径的相互作用促进细胞凋亡。
结论
KIF15作为一个早期预后基因，被鉴定为OC的候选组织病理学生物标志物和治疗靶点。
Zotero 插件