Kinesin 12 (KIF15) contributes to the development and tumorigenicity of prostate cancer

In Asia, prostate cancer is becoming a growing concern, impacting both socially and economically, compared with what is seen in western countries. Hence, it is essential to know the mechanisms associated with the development and tumorigenesis of PCa for primary diagnosis, risk management, and develo...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2021-10, Vol.576, p.7-14
Main Authors: Qureshi, Zeeshan, Ahmad, Mashaal, Yang, Wan-Xi, Tan, Fu-Qing
Format: Article
Language:English
Subjects:
Animals
Biomarkers, Tumor - genetics
Cell cycle
Cell Line, Tumor
Cell Movement - physiology
Cell Proliferation - physiology
Computational Biology - methods
Databases, Genetic
Humans
KIF15
Kinesins - genetics
Kinesins - metabolism
Male
MEK-ERK
Mice
Mice, Inbred BALB C
Mice, Nude
Proliferation
Prostate cancer
Prostatic Neoplasms - genetics
Prostatic Neoplasms - metabolism
Prostatic Neoplasms - pathology
Xenograft Model Antitumor Assays
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Summary:In Asia, prostate cancer is becoming a growing concern, impacting both socially and economically, compared with what is seen in western countries. Hence, it is essential to know the mechanisms associated with the development and tumorigenesis of PCa for primary diagnosis, risk management, and development of therapy strategies against PCa. Kinesin family member 15 (KIF15), a kinesin family member, is a plus-end-directed kinesin that functions to form bipolar spindles. There is emerging evidence indicating that KIF15 plays a significant role in several malignancies, such as pancreatic cancer, hepatocellular carcinoma, lung adenocarcinoma, and breast cancer. Still, the function of KIF15 remains unclear in prostate cancer. Here, we study the functional importance of KIF15 in the tumorigenesis of PCa. The bioinformatic analysis from PCa patients revealed high KIF15 expression compared to normal prostate tissues. High expression hinting at a possible functional role of KIF15 in regulating cell proliferation of PCa, which was demonstrated by both in vitro and in vivo assays. Downregulation of KIF15 silenced the expression of CDK2, p-RB, and Cyclin D1 and likewise blocked the cells at the G1 stage of the cell cycle. In addition, KIF15 downregulation inhibited MEK-ERK signaling by significantly silencing p-ERK and p-MEK levels. In conclusion, this study confirmed the functional significance of KIF15 in the growth and development of prostate cancer and could be a novel therapeutic target for the treatment of PCa. •Silencing of KIF15 inhibits proliferation and migration of PCa cell lines.•KIF15 suppression significantly arrested cells at the G1 phase of the cell cycle.•Downregulation of KIF15 resulted in altering the MEK-ERK pathway.•KIF15 inhibition in human PCa xenograft models delayed tumor initiation and growth.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2021.08.072