KIF4A: A potential biomarker for prediction and prognostic of  prostate cancer

Chen, Jiahong; Li, Maozhang; Fang, Shumin; Zhou, Xiaobo; Liao, Jinxian; Yang, Sheng-Bang; Zhu, Jianguo; He, Renqiang; Lü, Jianming; Jiang, Funeng; Xu, Xiaoming; Zhong, Weide

doi:10.25011/cim.v43i3.34393

Cited by 5 publications

(4 citation statements)

References 41 publications

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“…Kinesin superfamily 4 (kinesin family member 4, KIF4), a kind of interaction with microtubules, which also provides power for components in the cell movement of motor, which can make the microtubules to the cells at the pole movement, has many physiological functions 6,7 . KIF4A spinning cone in the late adjustment form and plays a key role in the process of mitosis; the anomaly can lead to abnormal mitosis checkpoint and DNA damage repair, and chromosome instability and the formation of aneuploidy, cause abnormal cell proliferation, differentiation and cause tumor formation 8,9 .…”

Section: Introductionmentioning

confidence: 99%

KIF4A enhanced cell proliferation and migration via Hippo signaling and predicted a poor prognosis in esophageal squamous cell carcinoma

et al. 2020

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Background In this study, we aimed to explore and clarify the function of KIF4A in esophageal squamous cell carcinoma (ESCC). Methods The microarray data were extracted from the Gene Expression Omnibus (GEO) database. We then used the database for Annotation, Visualization, and Integrated Discovery (DAVID) to perform the gene ontology function (GO) and KEGG Orthology‐Based Annotation System (KOBAS) to perform Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of differentially expressed genes (DEGs). The six core candidate genes were identified using protein–protein interaction (PPI) network analysis and Cytoscape software. Among them, the expression of KIF4A were validated by UALCAN database from the Cancer Genome Atlas (TCGA) (P < 0.05). Western blotting, qRT‐PCR and IHC were used to detect the expression of KIF4A in tissues. Cell experiments (transwell migration assays, wound healing assay, CCK8 assay, and clone formation experiment) were utilized to verify the roles of KIF4A on the ESCC cells. Western blotting was used to explore the mechanism of KIF4A in ESCC. Results The expression level of KIF4A was upregulated in ESCC samples compared to those in paracancerous tissues. Transwell migration and wound healing assay showed overexpression of KIF4A significantly promoted the migration of ESCC cells. CCK8 assay and clone formation experiment analysis showed that overexpression of KIF4A promoted proliferation of ESCC cells. Western blot detection found that KIF4A could affect the phosphorylation level of Hippo signaling pathway related proteins. Conclusions In summary, KIF4A promotes ESCC cell proliferation and migration by regulating the biological function of ESCC cells through the Hippo signaling pathway. Key points Significant findings of the study We found that high KIF4A expression was associated with poor overall survival in esophageal squamous cell carcinoma. KIF4A expression also promoted the proliferation and migration of ESCC cells in vitro. What this study adds Our experimental results explain the role of KIF4A in ESCC, and provide a new biomolecular target for the treatment of ESCC.

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Section: Introductionmentioning

confidence: 99%

KIF4A enhanced cell proliferation and migration via Hippo signaling and predicted a poor prognosis in esophageal squamous cell carcinoma

et al. 2020

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“…Moreover, the ic50 concentration of WZ-3146 (1nM) on glioma was used to detect the effect of WZ-3146 on HUVEC cells, the MTT results indicated that the HUVEC cell activity could not be effected by WZ-3146 at 1nM relative to control group, suggesting WZ-3146 had a specific inhibitory effect on glioma. To further explore the possible pathways affected by WZ-3146 in glioma, we analyzed the effects of KIF4A on glioma signaling pathways by GSEA and found that KIF4A significantly affects the apoptosis signaling pathway in glioma, consistent with the finding that KIF4A knockdown can induce prostate and ovarian cancer cell apoptosis [ 33 , 34 ]. Therefore, we further examined the effect of WZ-3146 on glioma cell apoptosis, and the results confirmed that WZ-3146 can significantly induce glioma cell apoptosis, which further confirmed that WZ-3146 can limit glioma progression by targeting KIF4A.…”

Section: Discussionmentioning

confidence: 56%

WZ-3146 acts as a novel small molecule inhibitor of KIF4A to inhibit glioma progression by inducing apoptosis

Yan,

Jiang,

et al. 2024

Cancer Cell Int

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Background Glioma is considered the most common primary malignant tumor of the central nervous system. Although traditional treatments have not achieved satisfactory outcomes, recently, targeted therapies for glioma have shown promising efficacy. However, due to the single-target nature of targeted therapy, traditional targeted therapies are ineffective; thus, novel therapeutic targets are urgently needed. Methods The gene expression data for glioma patients were derived from the GEO (GSE4290, GSE50161), TCGA and CGGA databases. Next, the upregulated genes obtained from the above databases were cross-analyzed, finally, 10 overlapping genes (BIRC5, FOXM1, EZH2, CDK1, KIF11, KIF4A, NDC80, PBK, RRM2, and TOP2A) were ultimately screened and only KIF4A expression has the strongest correlation with clinical characteristics in glioma patients. Futher, the TCGA and CGGA database were utilized to explore the correlation of KIF4A expression with glioma prognosis. Then, qRT-PCR and Western blot was used to detect the KIF4A mRNA and protein expression level in glioma cells, respectively. And WZ-3146, the small molecule inhibitor targeting KIF4A, were screened by Cmap analysis. Subsequently, the effect of KIF4A knockdown or WZ-3146 treatment on glioma was measured by the MTT, EdU, Colony formation assay and Transwell assay. Ultimately, GSEA enrichment analysis was performed to find that the apoptotic pathway could be regulated by KIF4A in glioma, in addition, the effect of WZ-3146 on glioma apoptosis was detected by flow cytometry and Western blot. Results In the present study, we confirmed that KIF4A is abnormally overexpressed in glioma. In addition, KIF4A overexpression is a key indicator of glioma prognosis; moreover, suppressing KIF4A expression can inhibit glioma progression. We also discovered that WZ-3146, a small molecule inhibitor of KIF4A, can induce apoptosis in glioma cells and exhibit antiglioma effects. Conclusion In conclusion, these observations demonstrated that targeting KIF4A can inhibit glioma progression. With further research, WZ-3146, a small molecule inhibitor of KIF4A, could be combined with other molecular targeted drugs to cooperatively inhibit glioma progression.

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“…KIF4A is involved in multiple cellular activities, particularly spindle formation and centrosome assembly in mitosis, chromosome concentration and separation, and DNA damage repair [ 17 ]. In addition, KIF4A is overexpressed in a variety of tumors [ 18 ]. A study on breast cancer established that ATAD2 could be recruited to the KIF4A promoter region by estrogen receptors alpha (ER α ) and other transcription factors to increase the transcription of KIF4A [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Aspirin Exerts Its Antitumor Effect in Esophageal Squamous Cell Carcinoma by Downregulating the Expression of ATAD2 and KIF4A

Zhang

Ren

Wang

et al. 2022

Analytical Cellular Pathology

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Objective. To investigate the expression of ATPase family AAA domain-containing protein 2 (ATAD2) and kinesin family member 4A (KIF4A) in esophageal squamous cell carcinoma (ESCC) tissues and their association with clinicopathological features and to explore the role of ATAD2 in regulating KIF4A expression and biological functions in ESCC cells and the effect of aspirin on their expression. Methods. The mRNA and protein expression of ATAD2 and KIF4A in the tissues of patients with ESCC were measured by RT-qPCR and immunohistochemistry, and the correlation between the expression of mRNA and clinicopathological characteristics was analyzed. Western blot and RT-qPCR were used to detect the interference efficiency and KIF4A expression after si-ATAD2 transfection in EC109 and KYSE30 cells. CCK-8 and Transwell assay were performed to investigate the effects of ATAD2 and aspirin on proliferation, migration, and invasion of ESCC cells. The effect of aspirin on the expression of ATAD2 and KIF4A in ESCC cells was measured by RT-qPCR and Western blot. Results. The expression of ATAD2 and KIF4A was upregulated in ESCC tissues, and both were correlated with the differentiation grades and lymph node metastasis. Knockdown of ATAD2 in ESCC cells significantly inhibited cell proliferation, migration, and invasion. Compared to the negative control group, the proliferation, migration, and invasion ability of ESCC cells in the aspirin-treated groups were decreased, and the expression of ATAD2 and KIF4A in ESCC cells was decreased after treating with aspirin for 48 h. Conclusion. The expression levels of ATAD2 and KIF4A are elevated in ESCC. ATAD2 promotes proliferation, migration, and invasion of ESCC cells by regulating KIF4A. Aspirin can inhibit the malignant behavior of ESCC cells by downregulating ATAD2 and KIF4A.

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KIF4A: A potential biomarker for prediction and prognostic of prostate cancer

Cited by 5 publications

References 41 publications

KIF4A enhanced cell proliferation and migration via Hippo signaling and predicted a poor prognosis in esophageal squamous cell carcinoma

KIF4A enhanced cell proliferation and migration via Hippo signaling and predicted a poor prognosis in esophageal squamous cell carcinoma

WZ-3146 acts as a novel small molecule inhibitor of KIF4A to inhibit glioma progression by inducing apoptosis

Aspirin Exerts Its Antitumor Effect in Esophageal Squamous Cell Carcinoma by Downregulating the Expression of ATAD2 and KIF4A

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