KIF20A promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the JAK/STAT3 signaling pathway.

Abstract:

BACKGROUND/AIMS:Kinesin family member 20A (KIF20A) is upregulated in multiple cancers and plays important roles in promoting malignant behavior, whereas its exact role in CRC remains unknown. RESULTS:Both genomic and protein expression levels showed that KIF20A was upregulated in CRC. Further functional analyses revealed that KIF20A had a crucial role in improving cell proliferation and resistance to chemotherapy in CRC. Finally, we provided distinct mechanistic evidence that KIF20A achieved all of its pathological functions in CRC by activating the JAK/STAT3 pathway. CONCLUSION:Our results suggested that KIF20A regulated a set of malignant characteristics in CRC by activating the JAK/STAT3 pathway. Our findings indicate a new direction for the development of more effective therapeutic treatments for CRC. METHODS:Three Gene Expression Omnibus datasets and The Cancer Genome Atlas datasets were used to investigate the expression level of KIF20A in CRC. Further experiments included immunohistochemical staining, western blot analysis, qRT-PCR, gene silencing, and a cell-injected xenograft mouse model to investigate the interaction between KIF20A and the JAK/STAT3 signaling pathway in both patient-derived specimens and CRC cell lines.

journal_name

Aging (Albany NY)

journal_title

Aging

authors

Xiong M,Zhuang K,Luo Y,Lai Q,Luo X,Fang Y,Zhang Y,Li A,Liu S

doi

10.18632/aging.102505

subject

Has Abstract

pub_date

2019-12-16 00:00:00

pages

11905-11921

issue

24

issn

1945-4589

pii

102505

journal_volume

11

pub_type

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