KIF4A promotes the development of bladder cancer by transcriptionally activating the expression of CDCA3
Bladder cancer (BC) is among the most common urinary system tumors with a high morbidity and mortality worldwide. Despite advancements being made in the diagnosis and treatment of bladder cancer, targeted therapy remains the most promising treatment, and novel therapeutic targets are urgently requir...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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D.A. Spandidos
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8041479/ https://www.ncbi.nlm.nih.gov/pubmed/33846765 http://dx.doi.org/10.3892/ijmm.2021.4932 |
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author | Zheng, Pengyi Wu, Kaijie Gao, Zhongwei Li, Huibing Li, Wensheng Wang, Xiaohui Shi, Zhenguo Xiao, Fei Wang, Kaixuan Li, Zhijun Han, Qingjiang |
author_facet | Zheng, Pengyi Wu, Kaijie Gao, Zhongwei Li, Huibing Li, Wensheng Wang, Xiaohui Shi, Zhenguo Xiao, Fei Wang, Kaixuan Li, Zhijun Han, Qingjiang |
author_sort | Zheng, Pengyi |
collection | PubMed |
description | Bladder cancer (BC) is among the most common urinary system tumors with a high morbidity and mortality worldwide. Despite advancements being made in the diagnosis and treatment of bladder cancer, targeted therapy remains the most promising treatment, and novel therapeutic targets are urgently required in to improve the outcomes of patients with BC. Kinesin family member 4A (KIF4A) is a plus-end directed motor protein involved in the regulation of multiple cellular processes, such as mitosis and axon growth. Notably, KIF4A plays important roles in tumor growth and progression, and its expression is associated with the prognosis of several types of cancer. However, the potential role and molecular mechanisms of KIF4A in bladder cancer development remain unclear. The present study demonstrated that KIF4A was highly expressed in human BC tissues, and its expression was associated with patient clinicopathological characteristics, such as tumor stage (P=0.012) and with the prognosis of patients with BC. It was further found that KIF4A promoted the cell proliferation of bladder cancer both in vitro and in vivo. On the whole, the data presented herein provide evidence that KIF4A promotes the development of BC through the transcriptional activation of the expression of CDCA3. The present study indicates the involvement of KIF4A in the progression of BC and suggests that KIF4A may be a promising therapeutic target for the treatment of BC. |
format | Online Article Text |
id | pubmed-8041479 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-80414792021-04-14 KIF4A promotes the development of bladder cancer by transcriptionally activating the expression of CDCA3 Zheng, Pengyi Wu, Kaijie Gao, Zhongwei Li, Huibing Li, Wensheng Wang, Xiaohui Shi, Zhenguo Xiao, Fei Wang, Kaixuan Li, Zhijun Han, Qingjiang Int J Mol Med Articles Bladder cancer (BC) is among the most common urinary system tumors with a high morbidity and mortality worldwide. Despite advancements being made in the diagnosis and treatment of bladder cancer, targeted therapy remains the most promising treatment, and novel therapeutic targets are urgently required in to improve the outcomes of patients with BC. Kinesin family member 4A (KIF4A) is a plus-end directed motor protein involved in the regulation of multiple cellular processes, such as mitosis and axon growth. Notably, KIF4A plays important roles in tumor growth and progression, and its expression is associated with the prognosis of several types of cancer. However, the potential role and molecular mechanisms of KIF4A in bladder cancer development remain unclear. The present study demonstrated that KIF4A was highly expressed in human BC tissues, and its expression was associated with patient clinicopathological characteristics, such as tumor stage (P=0.012) and with the prognosis of patients with BC. It was further found that KIF4A promoted the cell proliferation of bladder cancer both in vitro and in vivo. On the whole, the data presented herein provide evidence that KIF4A promotes the development of BC through the transcriptional activation of the expression of CDCA3. The present study indicates the involvement of KIF4A in the progression of BC and suggests that KIF4A may be a promising therapeutic target for the treatment of BC. D.A. Spandidos 2021-06 2021-04-09 /pmc/articles/PMC8041479/ /pubmed/33846765 http://dx.doi.org/10.3892/ijmm.2021.4932 Text en Copyright: © Zheng et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Zheng, Pengyi Wu, Kaijie Gao, Zhongwei Li, Huibing Li, Wensheng Wang, Xiaohui Shi, Zhenguo Xiao, Fei Wang, Kaixuan Li, Zhijun Han, Qingjiang KIF4A promotes the development of bladder cancer by transcriptionally activating the expression of CDCA3 |
title | KIF4A promotes the development of bladder cancer by transcriptionally activating the expression of CDCA3 |
title_full | KIF4A promotes the development of bladder cancer by transcriptionally activating the expression of CDCA3 |
title_fullStr | KIF4A promotes the development of bladder cancer by transcriptionally activating the expression of CDCA3 |
title_full_unstemmed | KIF4A promotes the development of bladder cancer by transcriptionally activating the expression of CDCA3 |
title_short | KIF4A promotes the development of bladder cancer by transcriptionally activating the expression of CDCA3 |
title_sort | kif4a promotes the development of bladder cancer by transcriptionally activating the expression of cdca3 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8041479/ https://www.ncbi.nlm.nih.gov/pubmed/33846765 http://dx.doi.org/10.3892/ijmm.2021.4932 |
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