Kinesin family member 23 (KIF23) contributes to the progression of bladder cancer cells in vitro and in vivo

Yao, Dongwei; Song, Qun; He, Xiaozhou

doi:10.4149/neo_2020_200803n808

Cited by 13 publications

(10 citation statements)

References 21 publications

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“…KIF23 depletion was reported to exert a promotive effect on apoptosis. 38,39 Here, knockdown of KIF23 partly antagonized the inhibitory effect of miR-17-5p inhibition on the apoptosis, ECM accumulation, and fibrosis in HMCs. Although KIF23 may function in cell proliferation and cell cycle due to its key task in mitosis and cytokinesis, this work only explored the role of KIF23 on apoptosis and fibrosis in MCs, which is a limitation of the present study.…”

Section: Inhibition Of Mir-17-5p Activates Wnt/β-catenin Signaling In Hmcs By Upregulating Kif23 Expressionmentioning

confidence: 86%

MiR‐17‐5p downregulation alleviates apoptosis and fibrosis in high glucose‐induced human mesangial cells through inactivation of Wnt/β‐catenin signaling by targeting KIF23

Chen

Cheng

et al. 2021

Environmental Toxicology

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Diabetic nephropathy (DN) remains the major cause of end-stage renal disease.MicroRNAs (miRNAs) have been reported to perform biological functions in many diseases. This investigation elucidated the biological role of miR-17-5p in DN. In this study, high glucose-cultured human mesangial cells (HMCs) were used as a cell model of DN. The miR-17-5p and KIF23 expression was measured by RT-qPCR. Cell apoptosis was detected by flow cytometry. The protein levels of apoptosis markers, fibrosis markers, and Wnt/β-catenin signaling-related genes were assessed using western blotting. The interaction of miR-17-5p with KIF23 was tested by a luciferase reporter assay. We found that miR-17-5p was upregulated in both DN patients and high glucose-treated HMCs. Silencing miR-17-5p attenuated the apoptosis and fibrosis in high glucose-treated HMCs. MiR-17-5p binds to KIF23 3 0 UTR and negatively regulates KIF23 expression. KIF23 knockdown could suppress the role of miR-17-5p inhibition in high glucose-treated HMCs. Additionally, inhibition of miR-17-5p activated Wnt/β-catenin signaling in HMCs through upregulating KIF23 expression. Suppression of Wnt/β-catenin signaling antagonized the effect of miR-17-5p in HMCs.In conclusion, miR-17-5p inhibition alleviates the apoptosis and fibrosis in high glucose-treated HMCs by targeting KIF23 activating Wnt/β-catenin signaling.

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Section: Inhibition Of Mir-17-5p Activates Wnt/β-catenin Signaling In Hmcs By Upregulating Kif23 Expressionmentioning

confidence: 86%

MiR‐17‐5p downregulation alleviates apoptosis and fibrosis in high glucose‐induced human mesangial cells through inactivation of Wnt/β‐catenin signaling by targeting KIF23

Chen

Cheng

et al. 2021

Environmental Toxicology

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“…Similarly, by regulating mitogenesis, KIF23 can influence cancer cell proliferation. Cell and animal experiments [ 44 ] confirmed the link between KIF23 and bladder cancer. According to the GSVA analysis and consensus clustering algorithm of “CancerSubtypes,” the high expression of gene set “GSE1460_CD4_THYMOCYTE_VS_THYMIC_STROMAL_CELL_DN” contributes to the poor prognosis of BLCA patients.…”

Section: Discussionmentioning

confidence: 99%

A Multiomics Profiling Based on Online Database Revealed Prognostic Biomarkers of BLCA

Chen

2022

BioMed Research International

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Background. Bladder cancer (BLCA) is one of the most common urological malignancies globally, posing a severe threat to public health. In combination with protein-protein interaction (PPI) network analysis of proteomics, Gene Set Variation Analysis (GSVA) and “CancerSubtypes” package of R software for transcriptomics can help identify biomarkers related to BLCA prognosis. This will have significant implications for prevention and treatment. Method. BLCA data were downloaded from The Cancer Genome Atlas (TCGA) database and GEO database (GSE13507). GSVA analysis converted the gene expression matrix to the gene set expression matrix. “CancerSubtypes” classified patients into three subtypes and established a prognostic model based on differentially expressed gene sets (DEGSs) among the three subtypes. For genes from prognosis-related DEGSs, functional and pathway enrichment analyses and PPI network analysis were carried out. The Human Protein Atlas (HPA) database was used for validation. Finally, the proportion of tumor-infiltrating immune cells (TIICs) was determined using the CIBERSORT algorithm. Results. In total, 414 tumor samples and 19 adjacent-tumor samples were obtained from TCGA, with 145 samples belonging to subtype A, 126 samples belonging to subtype B, and 136 samples belonging to subtype C. Then, we identified 83 DEGSs and constituted a prognostic signature with two of them: “GSE1460_CD4_THYMOCYTE_VS_THYMIC_STROMAL_CELL_DN” and “MODULE_253.” Finally, five subnets of two PPI networks were established, and nine core proteins were obtained: CDH2, COL1A1, EIF2S2, PSMA3, NAA10, DNM1L, TUBA4A, KIF11, and KIF23. The HPA database confirmed the expression of the nine core proteins in BLCA tissues. Furthermore, EIF2S2, PSMA3, DNM1L, and TUBA4A could be novel BLCA prognostic biomarkers. Conclusions. In this study, we discovered two gene sets linked to BLCA prognosis. PPI analysis confirmed the network’s core proteins, and several newly discovered biomarkers of BLCA prognosis were identified.

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“…For instance, KIF15 promotes hepatocellular carcinoma malignancy and cancer stem cell differentiation by remodeling the balance in reactive oxygen species ), and KIF18B expression exhibits a negative association with the prognosis and tumor grade of the colon adenocarcinoma (Zhao et al 2020). KIF23, the component of central spindling complex, has been con rmed to be involved in the cytokinesis(van de Ven et al 2016) and contribute to multiple cancers, including gastric carcinoma, primary and advanced lung cancer, pancreatic ductal adenocarcinoma, and bladder cancer (Gao et al 2020;Kato et al 2016;Liang et al 2020;Yao et al 2021). However, the potential association between KIF23 expression and NPC is unclear, and the mechanism underlying the function of KIF23 in NPC also warrants investigation.…”

Section: Introductionmentioning

confidence: 99%

KIF23, under regulation by androgen receptor, can promote the deterioration of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway

Liu

Zhang

et al. 2023

Preprint

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Our study aimed to explore the potential mechanisms of KIF23 regulating function in the progression of nasopharyngeal carcinoma and pinpoint novel therapeutic targets for the clinical treatment of nasopharyngeal carcinoma patients. The mRNA and protein level of KIF23 in nasopharyngeal carcinoma was measured using quantitative real-time PCR and western blot. The influence of KIF23 on tumor metastasis and growth in nasopharyngeal carcinoma was determined through the in vivo and in vitro experiments. The regulatory mechanisms of KIF23 in nasopharyngeal carcinoma were illustrated in the chromatin immunoprecipitation assay. KIF23 was found to be overexpressed in nasopharyngeal carcinoma samples, and its expression was associated with poor prognosis. Nasopharyngeal carcinoma cell’s proliferation, migration and invasion potential could be improved by inducing KIF23 expression both in vivo and in vitro. Androgen receptor (AR) was found to bind to the KIF23 promoter region directly and enhance KIF23 transcription. Furthermore, KIF23 could accelerate nasopharyngeal carcinoma deterioration via activating the Wnt/β-catenin signaling pathway. AR/KIF23/ Wnt/β-catenin pathway promotes nasopharyngeal carcinoma deterioration. Our findings could serve as a new therapeutic strategy for nasopharyngeal carcinoma in the clinical practice.

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Kinesin family member 23 (KIF23) contributes to the progression of bladder cancer cells in vitro and in vivo

Cited by 13 publications

References 21 publications

MiR‐17‐5p downregulation alleviates apoptosis and fibrosis in high glucose‐induced human mesangial cells through inactivation of Wnt/β‐catenin signaling by targeting KIF23

MiR‐17‐5p downregulation alleviates apoptosis and fibrosis in high glucose‐induced human mesangial cells through inactivation of Wnt/β‐catenin signaling by targeting KIF23

A Multiomics Profiling Based on Online Database Revealed Prognostic Biomarkers of BLCA

KIF23, under regulation by androgen receptor, can promote the deterioration of nasopharyngeal carcinoma by activating the Wnt/β-catenin signaling pathway

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