Publication: Downregulation of KIF15 inhibits the tumorigenesis of non-small-cell lung cancer via inactivating Raf/MEK/ERK signaling
Authors
Luo, Yingbin ; Zhang, Bo ; Xu, Lili ; Li, Minghua ; Wu, Jianchun ; Zhou, Yiyang ; Li, Yan
item.page.secondaryauthor
item.page.director
Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
publication.page.editor
publication.page.department
DOI
https://doi.org/10.14670/HH-18-408
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Background. Lung cancer is one of the most
common causes of cancer-associated mortality
worldwide. Upregulation of kinesin family member 15
(KIF15) expression has been observed in non-small cell
lung cancer (NSCLC), and high expression levels of
KIF15 are associated with a poor prognosis in patients
with NSCLC. However, to the best of our knowledge,
the mechanisms by which KIF15 regulates apoptosis,
migration and invasion in NSCLC remain unclear.
Methods. Cell Counting Kit-8, flow cytometry and
Transwell assays were performed to determine the
proliferation, apoptosis and invasion of NSCLC cells,
respectively. In addition, western blotting was used to
detect the levels of phosphorylated (p-)c-Raf, p-ERK
and p-MEK in NSCLC cells.
Results. Downregulation of KIF15 expression
markedly inhibited the proliferation, migration and
invasion of NSCLC cells through mediation of MMP2
and MMP9. In addition, downregulation of KIF15
markedly induced apoptosis and cell cycle arrest in
NSCLC cells through regulation of active caspase 3, p27
Kip1 and cyclin D1. Furthermore, KIF15 knockdown
notably decreased the levels of activating transcription
factor 2, p-c-Raf, p-ERK and p-MEK in A549 and NCIH460 cells. Finally, KIF15 knockdown notably inhibited
the tumor growth of NSCLC in vivo.
Conclusion. In conclusion, the present study
indicated that downregulation of KIF15 expression was
able to inhibit the tumorigenesis of NSCLC by
inactivating Raf/MEK/ERK signaling. These findings
may help improve the diagnosis and treatment of
NSCLC.
publication.page.subject
Citation
Histology and Histopathology Vol. 37, nº3 (2022)
item.page.embargo
Ir a EstadÃsticas
Este Ãtem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/