The role of kinesin KIF18A in the invasion and metastasis of hepatocellular carcinoma

Luo, Weiwei; Liao, Minjun; Liao, Yan; Chen, Xinhuang; Huang, Chunyan; Fan, Jiyuan; Liao, Weijia

doi:10.1186/s12957-018-1342-5

Cited by 52 publications

(43 citation statements)

References 24 publications

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“…Previous studies revealed that knockdown of KIF18A expression in human breast carcinoma cells caused increase of G2/M populations when compared with control RNAi cells . Recent study has also confirmed that the expression of cell cycle‐related protein such as cyclin B1 was decreased after knockdown of KIF18A in hepatocellular carcinoma . KIF18A might promote the malignant behavior, including proliferation, invasion, and metastasis by promoting cell cycle signaling pathways.…”

Section: Discussionmentioning

confidence: 82%

Overexpression of KIF18A promotes cell proliferation, inhibits apoptosis, and independently predicts unfavorable prognosis in lung adenocarcinoma

et al. 2019

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Kinesin family member 18A (KIF18A), as a member of the kinesin superfamily, is significantly overexpressed and abnormally functions in various human cancers. But, its expression profiling in the lung adenocarcinoma (LUAD) remains unclear. In the present work, using the data derived from the Cancer Genome Atlas (TCGA), we assessed the expression pattern and prognostic value of KIF18A in LUAD. In addition, we analyzed the underlying mechanism of its gene dysregulation. Experimental and bioinformatic analysis results showed that KIF18A expression was dramatically increased in LUAD tissues compared with the normal counterparts. Moreover, the patients with high KIF18A expression had significantly poorer overall survival (OS) and recurrence‐free survival (RFS). Univariate and multivariate analyses indicated that increased KIF18A expression was independently associated with unfavorable OS and RFS. In addition, by analyzing deep sequencing data from TCGA‐LUAD, we found that KIF18A mutation was detected in 2.6% of LUAD cases, and increased KIF18A expression was associated with genetic amplification rather than DNA methylation. Moreover, gene co‐expression network analysis revealed that a total of 339 KIF18A co‐expressed genes were detected and enriched in several tumor‐related pathways, especially cell cycle. Knockdown of KIF18A significantly inhibited cell proliferation in vitro and in vivo. Furthermore, silencing KIF18A induced LUAD cells apoptosis and arrested the cell cycle in the G2/M phase. KIF18A promotes cell proliferation, inhibits apoptosis, and is a valuable prognostic predictor and potential therapeutic target for the patients with LUAD. © 2019 IUBMB Life, 2019

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Section: Discussionmentioning

confidence: 82%

Overexpression of KIF18A promotes cell proliferation, inhibits apoptosis, and independently predicts unfavorable prognosis in lung adenocarcinoma

et al. 2019

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“…In this study, a large number of sample information analysis based on multiple data sets showed that KIF18A expression was increased in a variety of tumor tissues [13,15,[35][36][37] (Figure 1a), and the expression of KIF18A mRNA ( Figure 1b) and protein ( Figure 7) in glioma was signi cantly increased. Therefore, KIF18A expression was increased in gliomas, and its relationship with glioma and its function were further veri ed.…”

Section: Discussionmentioning

confidence: 62%

“…Notably, some recent reports suggest that KIF18A are also involved in the process of multiple tumors. Kif18A is associated with the occurrence and development of liver cancer [13], breast cancer [14], ovarian cancer [15] and can be used as potential biomarkers for breast cancer [16], colorectal [17] and hepatocellular carcinoma [18]. In contrast, the expression of kif18a is low in gastric cancer, which is associated with poor prognosis [19].…”

Section: Introductionmentioning

confidence: 99%

High Expression Levels of KIF18A is an Independent Predictor of Poor Survival in Glioma: A Study Using Multi Public Data

Chang¹,

Wang²,

Li³

et al. 2020

Preprint

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Background: Kinesin family member 18A (KIF18A) belongs to a member of the kinesin superfamily and is significantly overexpressed and abnormally functions in a variety of cancers. However, the expression profiling and the role of KIF18A has so far remained unclear in glioma. To investigate the relationship of KIF18A with clinical practice and its role in gliomas, the data from multi public datasets were used and analyzed in present study.Methods: Patients with gliomas were enrolled from CGGA RNA-seq, TCGA-seq, CGGA-microarray, GSE4290 and GSE50161 databases. The expression of KIF18A in glioma and normal tissues was analyzed through Wilcoxon rank sum test, and the relationship between KIF18A and clinicopathological features was evaluated using logistic regression. The effect of KIF18A expression in the survival of glioma patients was explored by Kaplan-Meier and Cox analyses. Gene set enrichment analysis was also conducted to annotate biological function of KIF18A.Results: KIF18A expression was significantly increased in glioma tissues compared with the normal counterparts. High KIF18A expression shortened the overall survival in all grades gliomas and the survival period of patients with WHO grade Ⅲ glioma, but not significantly for grade Ⅱ and grade Ⅳ glioma. Univariate and multivariate analyses demonstrated that evaluated KIF18A expression is closely related to poor prognosis. Increased KIF18A expression was significantly correlated grades, age, IDH wide type and may serve as a biomarker of poor prognosis in gliomas. GSEA showed that the KEGG_DNA_REPLICATION, the KEGG_CELL_CYCLE, the KEGG_MISMATCH_REPAIR and the KEGG_NUCLEOTIDE_EXCISION_REPAIR were differentially enriched in KIF18A high expression phenotype.Conclusions: High expression KIF18A might be potential biomarker for the diagnosis and an independent risk factor for poor prognosis in glioma.

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“…Since it was reported that Kif18a influences mouse germ cell proliferation (Czechanski et al, 2015;Luo et al, 2018;Zhong et al, 2019), we first investigated such potential effect of human KIF18A on TCam-2 cells, which originates from male germ cells. For that purpose we performed MTS proliferation assay upon KIF18A knockdown, starting at 24 h up to 120 h post transfection.…”

Section: Knockdown Of Kif18a Caused Decreased Tcam-2 Cell Proliferatimentioning

confidence: 99%

Kinesin KIF18A is a novel PUM regulated target promoting mitotic progression and survival of human male germ cell line - TCam-2

Smialek

Kuczyńska

Ilaslan

et al. 2019

Preprint

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Regulation of proliferation, apoptosis and cell cycle is crucial for the physiology of germ cells. Their malfunction contributes to infertility and germ cell tumours. Kinesin KIF18A is an important germ cell specific regulator which downregulates apoptosis while promoting cell proliferation in animal models. Whereas regulation of KIF18A expression was studied at the transcriptional level, its posttranscriptional regulation has not been extensively explored. Due to the presence of two PUM Binding Elements (PBEs) within 3'UTR, KIF18A mRNA is a potential target of PUMs, well known RNA-binding proteins involved in posttranscriptional gene regulation (PTGR). We investigated that possibility in TCam-2 cells originating from seminoma, representing human male germ cells. We conducted RNA co-immunoprecipitation combined with RT-qPCR, as well as luciferase reporter assay by applying appropriate luciferase construct encoding the wild type KIF18A 3'UTR, upon PUM1 and PUM2 overexpression or knockdown. We found that KIF18A is repressed by PUM1 and PUM2. To study how this regulation influences KIF18A function in TCam-2 cells, MTS proliferation assay, apoptosis and cell cycle, analysis using flow cytometry was performed upon KIF18A siRNA knockdown. We uncovered that KIF18A significantly influences proliferation, apoptosis and cell cycle, these effects being opposite to PUM effects in TCam-2 cells. We propose that repression by PUM proteins may represent one of mechanisms influencing KIF18A level in controlling proliferation, cell cycle and apoptosis in TCam-2 cells. To the best of our knowledge, this paper identifies the first mammalian functionally germ cell specific gene that is regulated by Pum proteins via 3'UTR.

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The role of kinesin KIF18A in the invasion and metastasis of hepatocellular carcinoma

Cited by 52 publications

References 24 publications

Overexpression of KIF18A promotes cell proliferation, inhibits apoptosis, and independently predicts unfavorable prognosis in lung adenocarcinoma

Overexpression of KIF18A promotes cell proliferation, inhibits apoptosis, and independently predicts unfavorable prognosis in lung adenocarcinoma

High Expression Levels of KIF18A is an Independent Predictor of Poor Survival in Glioma: A Study Using Multi Public Data

Kinesin KIF18A is a novel PUM regulated target promoting mitotic progression and survival of human male germ cell line - TCam-2

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