MCM family in HCC: MCM6 indicates adverse tumor features and poor outcomes and promotes S/G2 cell cycle progression View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-02-20

AUTHORS

Zhikun Liu, Jie Li, Jun Chen, Qiaonan Shan, Haojiang Dai, Haiyang Xie, Lin Zhou, Xiao Xu, Shusen Zheng

ABSTRACT

BackgroundMinichromosome Maintenance family (MCMs), as replication licensing factors, is involved in the pathogenesis of tumors. Here, we investigated the expression of MCMs and their values in hepatocellular carcinoma (HCC).MethodsMCMs were analyzed in 105 samples including normal livers (n = 15), cirrhotic livers (n = 40), HCC (n = 50) using quantitative polymerase chain reaction (qPCR) (Cohort 1). Significantly up-regulated MCMs were verified in 102 HCC and matched peritumoral livers using PCR (Cohort 2), and the correlations with clinical features and outcomes were determined. In addition, the focused MCMs were analyzed in parallel immunohistochemistry of 345 samples on spectrum of hepatocarcinogenesis (Cohort 3) and queried for the potential specific role in cell cycle.ResultsMCM2–7, MCM8 and MCM10 was significantly up-regulated in HCC in Cohort 1. In Cohort 2, overexpression of MCM2–7, MCM8 and MCM10 was verified and significantly correlated with each other. Elevated MCM2, MCM6 and MCM7 were associated with adverse tumor features and poorer outcomes. In Cohort 3, MCM6 exhibited superior HCC diagnostic performance compared with MCM2 and MCM7 (AUC: 0.896 vs. 0.675 and 0.771, P < 0.01). Additionally, MCM6 other than MCM2 and MCM7 independently predicted poorer survival in 175 HCC patients. Furthermore, knockdown of MCM6 caused a delay in S/G2-phase progression as evidenced by down-regulation of CDK2, CDK4, CyclinA, CyclinB1, CyclinD1, and CyclinE in HCC cells.ConclusionsWe analyze MCMs mRNA and protein levels in tissue samples during hepatocarcinogenesis. MCM6 is identified as a driver of S/G2 cell cycle progression and a potential diagnostic and prognostic marker in HCC. More... »

PAGES

200

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12885-018-4056-8

DOI

http://dx.doi.org/10.1186/s12885-018-4056-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1101139240

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29463213


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41 schema:description BackgroundMinichromosome Maintenance family (MCMs), as replication licensing factors, is involved in the pathogenesis of tumors. Here, we investigated the expression of MCMs and their values in hepatocellular carcinoma (HCC).MethodsMCMs were analyzed in 105 samples including normal livers (n = 15), cirrhotic livers (n = 40), HCC (n = 50) using quantitative polymerase chain reaction (qPCR) (Cohort 1). Significantly up-regulated MCMs were verified in 102 HCC and matched peritumoral livers using PCR (Cohort 2), and the correlations with clinical features and outcomes were determined. In addition, the focused MCMs were analyzed in parallel immunohistochemistry of 345 samples on spectrum of hepatocarcinogenesis (Cohort 3) and queried for the potential specific role in cell cycle.ResultsMCM2–7, MCM8 and MCM10 was significantly up-regulated in HCC in Cohort 1. In Cohort 2, overexpression of MCM2–7, MCM8 and MCM10 was verified and significantly correlated with each other. Elevated MCM2, MCM6 and MCM7 were associated with adverse tumor features and poorer outcomes. In Cohort 3, MCM6 exhibited superior HCC diagnostic performance compared with MCM2 and MCM7 (AUC: 0.896 vs. 0.675 and 0.771, P < 0.01). Additionally, MCM6 other than MCM2 and MCM7 independently predicted poorer survival in 175 HCC patients. Furthermore, knockdown of MCM6 caused a delay in S/G2-phase progression as evidenced by down-regulation of CDK2, CDK4, CyclinA, CyclinB1, CyclinD1, and CyclinE in HCC cells.ConclusionsWe analyze MCMs mRNA and protein levels in tissue samples during hepatocarcinogenesis. MCM6 is identified as a driver of S/G2 cell cycle progression and a potential diagnostic and prognostic marker in HCC.
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48 CDK4
49 ConclusionsWe
50 CyclinB1
51 G2 phase progression
52 HCC cells
53 HCC patients
54 MCM family
55 MCM2
56 MCM6
57 MCM7
58 MCM8
59 Mcm10
60 Mcm2-7
61 PCR
62 addition
63 adverse tumor features
64 carcinoma
65 cell cycle
66 cell cycle progression
67 cells
68 chain reaction
69 cirrhotic liver
70 clinical features
71 cohort 1
72 cohort 2
73 cohort 3
74 correlation
75 cycle
76 cycle progression
77 cyclinA
78 cyclinD1
79 cyclinE
80 delay
81 diagnostic performance
82 drivers
83 expression
84 factors
85 family
86 features
87 hepatocarcinogenesis
88 hepatocellular carcinoma
89 immunohistochemistry
90 knockdown
91 levels
92 licensing factors
93 liver
94 mRNA
95 markers
96 normal liver
97 outcomes
98 overexpression
99 parallel immunohistochemistry
100 pathogenesis
101 pathogenesis of tumors
102 patients
103 performance
104 peritumoral liver
105 polymerase chain reaction
106 poor outcome
107 poor survival
108 potential specific roles
109 prognostic marker
110 progression
111 protein levels
112 quantitative polymerase chain reaction
113 reaction
114 replication licensing factors
115 role
116 samples
117 specific role
118 spectra
119 survival
120 tissue samples
121 tumor features
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