Cargando…

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

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 func...

Descripción completa

Detalles Bibliográficos
Autores principales: Xiong, Man, Zhuang, Kangmin, Luo, Yunchen, Lai, Qiuhua, Luo, Xiaobei, Fang, Yuxin, Zhang, Yue, Li, Aimin, Liu, Side
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949076/
https://www.ncbi.nlm.nih.gov/pubmed/31841120
http://dx.doi.org/10.18632/aging.102505
_version_ 1783485845939945472
author Xiong, Man
Zhuang, Kangmin
Luo, Yunchen
Lai, Qiuhua
Luo, Xiaobei
Fang, Yuxin
Zhang, Yue
Li, Aimin
Liu, Side
author_facet Xiong, Man
Zhuang, Kangmin
Luo, Yunchen
Lai, Qiuhua
Luo, Xiaobei
Fang, Yuxin
Zhang, Yue
Li, Aimin
Liu, Side
author_sort Xiong, Man
collection PubMed
description 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.
format Online
Article
Text
id pubmed-6949076
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher Impact Journals
record_format MEDLINE/PubMed
spelling pubmed-69490762020-01-13 KIF20A promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the JAK/STAT3 signaling pathway Xiong, Man Zhuang, Kangmin Luo, Yunchen Lai, Qiuhua Luo, Xiaobei Fang, Yuxin Zhang, Yue Li, Aimin Liu, Side Aging (Albany NY) Research Paper 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. Impact Journals 2019-12-16 /pmc/articles/PMC6949076/ /pubmed/31841120 http://dx.doi.org/10.18632/aging.102505 Text en Copyright © 2019 Xiong et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Xiong, Man
Zhuang, Kangmin
Luo, Yunchen
Lai, Qiuhua
Luo, Xiaobei
Fang, Yuxin
Zhang, Yue
Li, Aimin
Liu, Side
KIF20A promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the JAK/STAT3 signaling pathway
title KIF20A promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the JAK/STAT3 signaling pathway
title_full KIF20A promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the JAK/STAT3 signaling pathway
title_fullStr KIF20A promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the JAK/STAT3 signaling pathway
title_full_unstemmed KIF20A promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the JAK/STAT3 signaling pathway
title_short KIF20A promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the JAK/STAT3 signaling pathway
title_sort kif20a promotes cellular malignant behavior and enhances resistance to chemotherapy in colorectal cancer through regulation of the jak/stat3 signaling pathway
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6949076/
https://www.ncbi.nlm.nih.gov/pubmed/31841120
http://dx.doi.org/10.18632/aging.102505
work_keys_str_mv AT xiongman kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway
AT zhuangkangmin kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway
AT luoyunchen kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway
AT laiqiuhua kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway
AT luoxiaobei kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway
AT fangyuxin kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway
AT zhangyue kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway
AT liaimin kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway
AT liuside kif20apromotescellularmalignantbehaviorandenhancesresistancetochemotherapyincolorectalcancerthroughregulationofthejakstat3signalingpathway