&lt;p&gt;Kinesin Superfamily Member 18B (KIF18B) Promotes Cell Proliferation in Colon Adenocarcinoma&lt;/p&gt;

Zhao, Fei; Feng, Yi; Zhang, Xueqiang; Liu, Xiaohui; Li, Aili

doi:10.2147/cmar.s261894

Cited by 12 publications

(13 citation statements)

References 28 publications

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“…Excessive proliferation of cells is closely related to the occurrence of tumors (Shi et al, 2020). Zhao et al (2020) found that the KIF18B promotes cell proliferation in colon adenocarcinoma and tumor growth in vitro and in vivo. In our research, we found that the ability and speed of CRC cells proliferation were slower in the KIFC3-depleted groups in the EdU assay, CCK-8 and colony formation assay.…”

Section: Discussionmentioning

confidence: 99%

“…The resulting daughter cells may exhibit cancerous behavior, including the ability of increased metastasis ( Almeida and Maiato, 2018 ; Lucanus and Yip, 2018 ). The invasion and migration of tumors are the main reasons leading to the failure of tumor treatment and poor prognosis, which cause low 5-year survival rates ( Zhan et al, 2020 ; Zhao et al, 2020 ). In tumorigenesis and metastasis, EMT plays a critical role.…”

Section: Discussionmentioning

confidence: 99%

“…KIF2A is overexpressed in squamous cell carcinoma of the oral tongue, and the downregulation of KIF2A can induce apoptosis in squamous cell carcinoma of the oral tongue through the inhibition of the PI3K/AKT signaling pathway ( Wang et al, 2014 ). KIF18B is highly expressed in colon adenocarcinoma tissues and negatively correlated with patients’ prognosis ( Zhao et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

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KIFC3 Promotes Proliferation, Migration, and Invasion in Colorectal Cancer via PI3K/AKT/mTOR Signaling Pathway

Liao

Zhang

et al. 2022

Front. Genet.

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Background: KIFC3, belongs to kinesin superfamily proteins (KIFs), is well known for its role in intracellular cargo movement. KIFC3 has been identified as a docetaxel resistance gene in breast cancer cells, however, the role of KIFC3 and its potential mechanism in colorectal cancer (CRC) remains elusive.Objectives: We aims to investigate the effects of KIFC3 in proliferation, migration, and invasion in CRC as well as the potential mechanism inside.Methods: We investigated the expression of KIFC3 in the Oncomine, Gene Expression Profiling Interactive Analysis databases. The KIFC3 protein expression and mRNA level in CRC cells were evaluated by western blot and qRT-PCR. Cell proliferation ability was detected by CCK-8, EdU, colony formation assay and xenograft tumor in nude mice. Flow cytometry was used to detect the cell cycle. The effect of KIFC3 on the epithelial-to-mesenchymal transition (EMT) was investigated by transwell and wound healing assay. The association of KIFC3 with EMT and PI3K/AKT/mTOR signaling pathway were measured by western blot and immunofluorescence staining.Results: The expression of KIFC3 was higher in CRC tissues than normal colorectal tissue, and was negatively correlated with the overall survival of patients with CRC. KIFC3 silencing inhibited the proliferation, migration and invasion of CRC cells. Meanwhile, it could decrease the number of cells in S phase. KIFC3 silencing inhibited the expression of proliferating cell nuclear antigen, Cyclin A2, Cyclin E1, and CDK2 and increased the expression of p21 and p53. KIFC3 overexpression promoted the G1/S phase transition. KIFC3 silencing inhibited the EMT process, which decreased the level of N-cadherin, Vimentin, SNAIL 1, TWIST, MMP-2, MMP-9 and increased E-cadherin, while KIFC3 overexpression show the opposite results. Furthermore, the knockdown of KIFC3 suppressed the EMT process by modulating the PI3K/AKT/mTOR signaling pathway. KIFC3 silencing decreased the expression of phosphorylated PI3K, AKT, mTOR, but total PI3K, AKT, mTOR have no change. Inversely, the upregulation of KIFC3 increased the expression of phosphorylated PI3K, AKT and mTOR, total PI3K, AKT, mTOR have no change. In a xenograft mouse model, the depletion of KIFC3 suppressed tumor growth. the increased expression levels of KIFC3 could enhance the proliferation, migration and invasion of CRC cells, and enhance the EMT process through the PI3K/AKT/mTOR pathway.Conclusion: Our study substantiates that KIFC3 can participate in the regulation of CRC progression by which regulates EMT via the PI3K/AKT/mTOR axis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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KIFC3 Promotes Proliferation, Migration, and Invasion in Colorectal Cancer via PI3K/AKT/mTOR Signaling Pathway

Liao

Zhang

et al. 2022

Front. Genet.

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“…Previous studies demonstrated KIFs were involved in different types of cancers [ 5 ]. For example, KIF15 can promote cancer stem cell phenotype in hepatocellular carcinoma [ 10 ], while KIF18B can promote cell proliferation in hepatocellular carcinoma [ 11 ]. In addition, several studies have illustrated KIF23 participates in the occurrence of multiple cancers, including gastric cancer, bladder cancer, lung cancer and pancreatic ductal adenocarcinoma [ 12 – 16 ].…”

Section: Introductionmentioning

confidence: 99%

Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway

Yang

Zhang

et al. 2022

J Exp Clin Cancer Res

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Background Triple negative breast cancer (TNBC) is highly malignant and has a worse prognosis, compared with other subtypes of breast cancer due to the absence of therapeutic targets. KIF23 plays a crucial role in the tumorigenesis and cancer progression. However, the role of KIF23 in development of TNBC and the underlying mechanism remain unknown. The study aimed to elucidate the biological function and regulatory mechanism of KIF23 in TNBC. Methods Quantitative real-time PCR and Western blot were used to determine the KIF23 expression in breast cancer tissues and cell lines. Then, functional experiments in vitro and in vivo were performed to investigate the effects of KIF23 on tumor growth and metastasis in TNBC. Chromatin immunoprecipitation assay was conducted to illustrate the potential regulatory mechanisms of KIF23 in TNBC. Results We found that KIF23 was significantly up-regulated and associated with poor prognosis in TNBC. KIF23 could promote TNBC proliferation, migration and invasion in vitro and in vivo. KIF23 could activate Wnt/β-catenin pathway and promote EMT progression in TNBC. In addition, FOXM1, upregulated by WDR5 via H3K4me3 modification, directly bound to the promoter of KIF23 gene to promote its transcription and accelerated TNBC progression via Wnt/β-catenin pathway. Both of small inhibitor of FOXM1 and WDR5 could inhibit TNBC progression. Conclusions Our findings elucidate WDR5/FOXM1/KIF23/Wnt/β-catenin axis is associated with TNBC progression and may provide a novel and promising therapeutic target for TNBC treatment.

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“…Kinesin superfamily proteins (also known as KIFs) are important molecular motors that directionally transport various cargos, including membranous organelles, protein complexes and mRNAs [7] . The mechanisms how different kinesins recognize and bind to speci c cargos, as well as how determine the direction of transport and kinesins unload cargo, have already been revealed [8][9][10] . And KIFs also play an important role in the process of tumor proliferation, invasion and metastasis.Li et al reported KIF2C/4A/10/11/14/18B/20A/23 predict poor prognosis and promote cell proliferation in hepatocellular carcinoma [11] .…”

Section: Introductionmentioning

confidence: 99%

KIF11 Might be a Novel Biomarker for Bone Metastasis of Prostate Adenocarcinoma

Wang¹,

Li²,

Liu³

et al. 2021

Preprint

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Background: A serious issue derived from Prostate adenocarcinoma (PCa) is its propensity to metastasize to bone, which occurred in up to 90% of patients with advanced PCa. The kinesin superfamily (KIFs) is well-documented oncogenic protein implicated mainly in chromosomal and spindle movements and are involved in some cellular activities, such as mitosis, transport of vesicles, organelles, and mRNAs. However, the clinical significance and biological roles of KIF in bone metastasis of PCa still need further exploration.Method: We download three datasets from the Gene Expression Omnibus (GEO) data repository. Firstly, we merge the three datasets, and then obtain the gene modules most relevant with clinical traits(morbidity of the bone metastasis of PCa) by “WGCNA” R package. Functional enrichment analysis was performed by the DAVID tool and Metascape. Differentially expressed genes (DEGs) between bone metastasis of PCa and primary PCa tissue samples were identified by “limma” R package. Then we intersect the gene module with DEGs. Protein-protein interaction (PPI) network was constructed by Cytoscape, and hub genes were excavated. Immunohistochemistry (IHC) image was downloaded from The Human Protein Atlas (www.proteinatlas.org) to verify the feasibility of the target molecular marker identified by bioinformatics and statistical analysis.Result:16 gene modules were obtained through WGCNA analysis and the tan module is most related to the occurrence of bone metastasis, containing 147 genes. Thus, we selected the tan module for further analysis. 877 DEGs were detected by limma package of R software. After taking the intersection of the DEGs and tan module, we got 51 common genes. Protein-protein interaction network (PPI) was constructed for the 51 genes. 7 hub genes (BUB1, KIF2C, RACGAP1, CENPE, KIF11, TTK, KIF20A) were identified from the common results of four different algorithms (Betweenness, Closeness, EcCentricity, and Radiality). Survival analysis based on disease free survival (DFS) was carried out for the 7 hub genes, and all of them have significant poor prognostic performance (P<0.05). And the bubble charts were plotted for functional annotation of the miRNA which can be the regulating factors of the hub genes. Univariate and multivariate logistic regression analysis were performed for screening the independent risk factors of the bone metastasis of PCa, and KIF11 was finally obtained. The immunohistochemical image of bone metastasis of PCa was obtained on the protein Atlas, which showed a strong positive expression of KIF11.Conclusion: In current study, molecules strongly correlated with the occurrence of bone metastasis of PCa were excavated. And provide the evidence that KIF11 may serve as a potential bone metastasis marker in PCa, which might be used for the guidance of clinical practice.

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<p>Kinesin Superfamily Member 18B (KIF18B) Promotes Cell Proliferation in Colon Adenocarcinoma</p>

Cited by 12 publications

References 28 publications

KIFC3 Promotes Proliferation, Migration, and Invasion in Colorectal Cancer via PI3K/AKT/mTOR Signaling Pathway

KIFC3 Promotes Proliferation, Migration, and Invasion in Colorectal Cancer via PI3K/AKT/mTOR Signaling Pathway

Kinesin family member 23, regulated by FOXM1, promotes triple negative breast cancer progression via activating Wnt/β-catenin pathway

KIF11 Might be a Novel Biomarker for Bone Metastasis of Prostate Adenocarcinoma

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