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DTYMK promote hepatocellular carcinoma proliferation by regulating cell cycle
Cell Cycle ( IF 4.3 ) Pub Date : 2021-08-09 , DOI: 10.1080/15384101.2021.1958502
Tianhao Zhou 1, 2 , Rui Qin 3 , Susu Shi 4 , Hua Zhang 3 , Chuanling Niu 3 , Gaoda Ju 4 , Sen Miao 3
Affiliation  

ABSTRACT

Overexpression of DTYMK is related with tumorigenesis and progression in several human tumors. However, the role of upregulated DTYMK in hepatocellular carcinoma (HCC) patients still remains unclear. In this study, the DTYMK expression in HCC tumors was evaluated in three GEO series (GSE14520, GSE54236, GSE63898), TCGA-LIHC, and ICGC-IRLR-JP cohorts. Survival analysis of DTYMK based on TCGA-LIHC and ICGC-LIRI-JP cohorts was conducted. We found that DTYMK was dramatically upregulated in tumor tissue compared with that in adjacent liver tissue. Kaplan-Meier analysis revealed that high expression of DTYMK in HCC patients’ tumor tissue was significantly corresponded to worse overall survival (OS) (P < 0.05). Further analysis showed that overexpressing DTYMK led to poor relapse free survival (RFS) and disease-specific survival (DSS) (all P < 0.05). In conclusion, DTYMK is upregulated in tumors and correlated with poor prognosis in HCC patients. In our report, DTYMK is higher expression in HCC cancer tissue and cell line than tumor adjacent tissue and normal liver cell line. Knocking down DTYMK can inhabit tumor cell proliferation by interfering cell cycle, whereas overexpression of DTYMK can promote tumor cell proliferation. These findings indicate that upregulation of DTYMK enhances tumor growth and proliferation by promoting cell cycle.



中文翻译:

DTYMK通过调节细胞周期促进肝癌增殖

摘要

DTYMK 的过表达与几种人类肿瘤的肿瘤发生和进展有关。然而,上调的 DTYMK 在肝细胞癌 (HCC) 患者中的作用仍不清楚。在本研究中,在三个 GEO 系列(GSE14520、GSE54236、GSE63898)、TCGA-LIHC 和 ICGC-IRLR-JP 队列中评估了 HCC 肿瘤中的 DTYMK 表达。进行了基于 TCGA-LIHC 和 ICGC-LIRI-JP 队列的 DTYMK 生存分析。我们发现与相邻肝组织相比,DTYMK 在肿瘤组织中显着上调。Kaplan-Meier 分析显示,HCC 患者肿瘤组织中 DTYMK 的高表达与较差的总生存期(OS)显着对应(P < 0.05)。进一步分析表明,过表达 DTYMK 导致无复发生存期 (RFS) 和疾病特异性生存期 (DSS) 较差(均 P < 0. 05)。总之,DTYMK 在肿瘤中上调并与 HCC 患者的不良预后相关。在我们的报告中,DTYMK 在 HCC 癌组织和细胞系中的表达高于肿瘤邻近组织和正常肝细胞系。敲低DTYMK可以通过干扰细胞周期抑制肿瘤细胞增殖,而过表达DTYMK可以促进肿瘤细胞增殖。这些发现表明 DTYMK 的上调通过促进细胞周期来增强肿瘤的生长和增殖。而 DTYMK 的过表达可以促进肿瘤细胞增殖。这些发现表明 DTYMK 的上调通过促进细胞周期来增强肿瘤的生长和增殖。而 DTYMK 的过表达可以促进肿瘤细胞增殖。这些发现表明 DTYMK 的上调通过促进细胞周期来增强肿瘤的生长和增殖。

更新日期:2021-09-28
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