KIF15 knockdown suppresses gallbladder cancer development

• DOI: 10.1016/j.ejcb.2021.151182
• Publication Date: 2021-11-05T21:50:59Z
• Authors: Jun Wang; Dandan Wang; Zhewei Fei; Dongxu Feng; Bo Zhang; Pingfa Gao; Gangfeng Hu; Wenbing Li; Xia Huang; Dawei Chen; Xinde Ding; Wei Wu
• Keywords: 0303 health sciences; Molecular target; QH573-671; Proliferation; Kinesins; Apoptosis; Gallbladder cancer; 3. Good health; Gene Expression Regulation, Neoplastic; Mice; Phosphatidylinositol 3-Kinases; 03 medical and health sciences; KIF15; Cell Line, Tumor; Animals; Humans; Gallbladder Neoplasms; Cytology; Migration; Cell Proliferation

Gallbladder cancer (GBC) is commonly regarded as one of the most lethal malignant tumor types with poor prognosis. Kinesin family member 15 (KIF15) reported to be tightly related progression multiple which, however, has not been clarified in GBC so far. KIF15 was significantly up-regulated clinical tissues compared that para-carcinoma and expression level also correlated malignancies. In addition tissues, cells exhibited a high abundance KIF15. After down-regulating via lentiviral transfection, cell proliferation migration were both inhibited, while apoptosis promoted markedly. Likewise, silencing interfered growth nude mouse xenografts. Our experiments lines demonstrated overexpression accelerated but lessened GBC-SD SGC-996 cells. Further investigation mechanism occurring inhibition mediated by knockdown revealed deficiency led decreased activity several signaling pathways (TNF, PI3K/AKT MAPK), reduction CDK6 regulated enhanced p21, HSP60 absence. Following treatment shCtrl- shKIF15-transfected AKT activator, we found anti-tumor effects resulting from could relieved activator experimental Overall, for first time, overexpressed displayed close relationship between levels stages. Furthermore, low resulted obvious effects.