High kinesin family member 18A expression correlates with poor prognosis in primary lung adenocarcinoma.

Lung adenocarcinoma (LUAD) is the most prevalent pathological subtype of lung cancer. Kinesin family member 18A (KIF18A) plays an important role in tumorigenesis. Its roles in breast cancer, colorectal cancer, and other tumors have been demonstrated; however, studies of KIF18A in LUAD are limited. This study aimed to determine the role of KIF18A in LUAD progression and prognostic prediction. KIF18A expression was examined in LUAD cells and tissues by immunohistochemistry and Western blotting. Cell proliferation assay was performed to study the role of KIF18A in LUAD cells. Correlations between KIF18A expression and clinicopathological features were analyzed. The role of KIF18A in LUAD prognosis was evaluated using data from The Cancer Genome Atlas (TCGA). KIF18A expression was increased in tumor cells and tissues. Downregulation of KIF18A expression resulted in the suppression of cancer cell proliferation in in vitro assays, and was particularly related to poor tumor differentiation, big tumor size, lymph node metastasis, and more advanced tumor stage. In the TCGA dataset, high KIF18A messenger RNA expression was associated with poor disease-free and overall survival in patients with LUAD. In addition, multivariate analysis indicated that KIF18A is an independent prognostic factor of disease-free and overall survival in LUAD. Collectively, our results demonstrate that KIFl8A is highly expressed in LUAD. KIFl8A plays an important role in LUAD cell proliferation, but is a poor prognostic factor.

Li X ，Liu M ，Zhang Z ，Zhang L ，Liang X ，Sun L ，Zhong D ... -  《-》

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

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.

Zhong Y ，Jiang L ，Lin H ，Li X ，Long X ，Zhou Y ，Li B ，Li Z ... -  《-》

Overexpression of KIF20A confers malignant phenotype of lung adenocarcinoma by promoting cell proliferation and inhibiting apoptosis.

Increasing studies showed that kinesin family member 20A (KIF20A) was overexpessed in several types of cancer, and its overexpression correlated with the oncogenesis and prognosis of cancers. However, little is known about the role of KIF20A in lung adenocarcinoma (LUAD). In this study, we employed the bioinformatics analysis to identify the upregulation of KIF20A in LUAD, then verified the results in human tumor specimens and LUAD cell lines. Compared with normal lung tissues, a ubiquitous upregulation of KIF20A was observed in LUAD tissues by immunohistochemistry (IHC) as well as TCGA analysis. Higher expression of KIF20A was significantly associated with more advanced clinicopathological features and shorter overall survival (OS). Moreover, multivariate Cox regression analysis revealed that KIF20A was an independent prognostic factor for OS. The expression of KIF20A was significantly elevated in LUAD cell lines. After silencing KIF20A, lung cancer cell cycle arrested in G1 phase and apoptosis increased. The same results were observed in vivo. Thus, our study demonstrated that KIF20A might confer malignant phenotype to LUAD by regulating cell proliferation and apoptosis, providing a new potential biomarker for clinical treatment of LUAD.

Zhao X ，Zhou LL ，Li X ，Ni J ，Chen P ，Ma R ，Wu J ，Feng J ... -  《Cancer Medicine》

Genome‑wide investigation of the clinical significance and prospective molecular mechanisms of kinesin family member genes in patients with lung adenocarcinoma.

Zhang L ，Zhu G ，Wang X ，Liao X ，Huang R ，Huang C ，Huang P ，Zhang J ，Wang P ... -  《-》

Co-expression network analysis identified KIF2C in association with progression and prognosis in lung adenocarcinoma.

Bai Y ，Xiong L ，Zhu M ，Yang Z ，Zhao J ，Tang H ... -  《-》