KIF11 Functions as an Oncogene and Is Associated with Poor Outcomes from Breast Cancer
- Author:
Juan ZHOU
1
;
Wei Rong CHEN
;
Li Chao YANG
;
Jun WANG
;
Jia Yuan SUN
;
Wen Wen ZHANG
;
Zhen Yu HE
;
San Gang WU
Author Information
- Publication Type:Original Article
- Keywords: Breast neoplasms; KIF11; Survival; Oncogenes
- MeSH: AMP-Activated Protein Kinases; Animals; Apoptosis; Blotting, Western; Breast Neoplasms; Breast; Cadherins; Cell Survival; Gene Expression; Genome; Humans; In Vitro Techniques; Mice; Mice, Nude; Oncogenes; Phosphorylation; Prognosis; Real-Time Polymerase Chain Reaction; Vimentin; Weights and Measures
- From:Cancer Research and Treatment 2019;51(3):1207-1221
- CountryRepublic of Korea
- Language:English
- Abstract: PURPOSE: The study aimed to search and identify genes that were differentially expressed in breast cancer, and their roles in cancer growth and progression. MATERIALS AND METHODS: The Gene Expression Omnibus (Oncomine) and The Cancer Genome Atlas databases (https://cancergenome.nih.gov/) were screened for genes that were expressed differentially in breast cancer and were closely related to a poor prognosis. Gene expressions were verified by quantitative real-time polymerase chain reaction, and genes were knocked down by a lentivirus-based system. Cell growth and motility were evaluated and in vivo nude mice were used to confirm the in vitro roles of genes. Markers of epithelial-to-mesenchymal transition and the associations of KIF11 with the classical cancer signaling pathways were detected by Western blot. RESULTS: A series of genes expressed differentially in patients with breast cancer. The prognosis associated with high KIF11 expression was poor, and the expression of KIF11 increased significantly in high stage and malignant tumor cells. Inhibiting KIF11 expression in lentivirus-suppressed cells revealed that KIF11 inhibition significantly reduced cell viability and colony formation, inhibited migration and invasion, but promoted apoptosis. The sizes and weights of KIF11-inhibited tumors in nude mice were significantly lower than in the negative controls. Western blot showed that E-cadherin in breast cancer was significantly upregulated in KIF-inhibited cells and tumor tissues, whereas N-cadherin and vimentin were significantly down-regulated. BT549 and MDA231 cells with KIF11 knockdown exhibited decreased ERK, AMPK, AKT, and CREB phosphorylation. CONCLUSION: KIF11 acts as a potential oncogene that regulates the development and progression of breast cancer.
