Expression and Clinical Role of Cdc5L as a Novel Cell Cycle Protein in Hepatocellular Carcinoma

Qiu, Huiyuan; Zhang, Xiubing; Ni, Wenkai; Shi, Weidong; Xu, Jian; Chen, Yongmei; Ni, Runzhou; Tao, Tao

doi:10.1007/s10620-015-3937-9

Cited by 24 publications

(20 citation statements)

References 30 publications

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“…Cell division cycle 5-like (CDC5L) is a cell cycle regulatory element of G2/M transformation and is involved in the catalytic steps of mRNA splicing and DNA damage repair. Studies indicated that CDC5L expression in glioma and hepatocellular carcinoma was increased, and CDC5L interference could increase the cell cycle arrest in G2 phase and inhibit the proliferation of glioma cells and hepatoma cells [15,16]. However, CDC5L has not been studied in MM.…”

Section: Introductionmentioning

confidence: 99%

ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L

Liu

Guo

Sha

et al. 2020

Aging

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This study aimed to investigate whether annexin A7 (ANXA7) could promote the cell cycle, proliferation and cell adhesion-mediated drug resistance (CAM-DR) of multiple myeloma (MM) cells by up-regulating cell division cycle 5-like (CDC5L). As a result, ANXA7 expression was increased in the serum of MM patients and the expression of ANXA7 and CDC5L was also increased in MM cell lines. ANXA7 overexpression promoted the proliferation and cycle of U266 and RPMI8226 cells. The expression of proliferation cell nuclear antigen (PCNA), KI67, cyclin dependent kinase 1 (CDK1) and cyclinB1 in transfected cells was consistent with the changes of proliferation and cell cycle. In co-culture system of BMSC cells and MM cells, expression of CD44, ICAM1 and VCAM1 in MM cells was increased, which was further increased by ANXA7 overexpression. Bortezomib could increase the apoptosis of U266 and RPMI8226 cells. In co-culture system of BMSC cells and MM cells, the promotion effects of bortezomib on apoptosis of MM cells was decreased, which was further suppressed by ANXA7 overexpression. The above effects exerted by ANXA7 overexpression could be reversed by ANXA7 interference. Moreover, ANXA7 was proved to be combined with CDC5L. CDC5L interference could inhibit the promotion effects of ANXA7 overexpression on proliferation and cell cycle and inhibition effects of ANXA7 overexpression on apoptosis of MM cells treated with bortezomib in co-culture system. In conclusion, ANXA7 could promote the cell cycle, proliferation and CAM-DR of MM cells by upregulating CDC5L.

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Section: Introductionmentioning

confidence: 99%

ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L

Liu

Guo

Sha

et al. 2020

Aging

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“…Overexpression of Cdc5L in mammalian cells causes shorter G2 phase and reduced cell size [16] and knockdown of Cdc5L results in dramatic mitotic arrest [17] and chromosome misalignments [18]. Recently, both Prp19 and Cdc5L have been characterized to be overexpressed in HCC tissues and their overexpression are positively correlated with poor prognosis [17,19]. Considering the importance of Prp19 and Cdc5L within this complex, the relationship between them deserves to be investigated in HCC.…”

Section: Introductionmentioning

confidence: 99%

Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells

Huang

Xue

et al. 2017

IJMS

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Pre-mRNA processing factor 19 (Prp19) is involved in many cellular events including pre-mRNA processing and DNA damage response. Recently, it has been identified as a candidate oncogene in hepatocellular carcinoma (HCC). However, the role of Prp19 in tumor biology is still elusive. Here, we reported that Prp19 arrested cell cycle in HCC cells via regulating G2/M transition. Mechanistic insights revealed that silencing Prp19 inhibited the expression of cell division cycle 5-like (Cdc5L) via repressing the translation of Cdc5L mRNA and facilitating lysosome-mediated degradation of Cdc5L in HCC cells. Furthermore, we found that silencing Prp19 induced cell cycle arrest could be partially resumed by overexpressing Cdc5L. This work implied that Prp19 participated in mitotic progression and thus could be a promising therapeutic target of HCC.

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“…High expression of CDC5L was an independent prognostic factor for poor survival of HCC patients. In vitro studies showed that overexpression of CDC5L contributed to cell cycle progress of HCC cells, while down-regulation of CDC5L resulted in cell cycle arrest at G2/M phase and reduced cell proliferation of HCC cells [26]. Moreover, higher phosphorylation of CDC5L was found in HCC cell line, MHCC97-H (high metastasis), indicating that it may participate in the metastasis of HCC [27].…”

Section: Discussionmentioning

confidence: 98%

Prognostic value of aberrantly expressed methylation genes in human hepatocellular carcinoma

Zhen

Ning

et al. 2020

Bioscience Reports

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Objectives: To identify the prognostic value of aberrantly methylated differentially expressed genes (DEGs) in hepatocellular carcinoma (HCC) and to explore the underlying mechanisms of tumorigenesis. Methods: Gene expression profiles (GSE65372 and GSE37988) were analyzed using GEO2R to obtain aberrantly methylated DEGs. Functional enrichment analysis of screened genes was performed by the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Cytoscape software was used to analyze the PPI network and to select hub genes. Transcriptional and proteinic expression data of hub genes were obtained through UALCAN and the Human Protein Reference Database. Finally, we analyzed the prognostic value of hub genes with the Kaplan-Meier Plotter and MethSurv database. Results: In total, 24 up-hypomethylated oncogenes and 37 down-hypermethylated tumor suppressor genes (TSGs) were identified, and 8 hub genes, including 4 up-hypomethylated oncogenes (CDC5L, MERTK, RHOA and YBX1) and 4 down-hypermethylated TSGs (BCR, DFFA, SCUBE2, TP63), were selected by PPI. Higher expression of methylated CDC5L-cg05671347, MERTK-cg08279316, RHOA-cg05657651 and YBX1-cg16306148, and lower expression of methylated BCR-cg25410636, DFFA-cg20696875, SCUBE2-cg19000089 and TP63-cg06520450, were associated with better overall survival (OS) in HCC patients. Multivariate analysis also showed they were independent prognostic factors for OS of HCC patients. Conclusions: In summary, different expression of methylated genes above mentioned were associated with better prognosis in HCC patients. Altering the methylation status of these genes may be a therapeutic target for HCC, but it should be further evaluated in clinical studies.

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Expression and Clinical Role of Cdc5L as a Novel Cell Cycle Protein in Hepatocellular Carcinoma

Abstract: Our findings suggested that Cdc5L could play an important role in the tumorigenesis of HCC and thus be a potential therapeutical target to prevent HCC progression.

Cited by 24 publications

References 30 publications

ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L

ANXA7 promotes the cell cycle, proliferation and cell adhesion-mediated drug resistance of multiple myeloma cells by up-regulating CDC5L

Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells

Prognostic value of aberrantly expressed methylation genes in human hepatocellular carcinoma

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