Overexpression of the structural maintenance of chromosome 4 protein is associated with tumor de-differentiation, advanced stage and vascular invasion of primary liver cancer

Zhou, Bo; Yuan, Tao; Liu, Menggang; Li, Hongming; Xie, Jun; Shen, Yifeng; Chen, Ping

doi:10.3892/or.2012.1929

Cited by 48 publications

(54 citation statements)

References 30 publications

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“…Previous studies have shown that the expression of SMC4 mRNA and protein was highly upregulated in HCC tissues and cell lines. Levels of SMC4 protein were significantly associated with tumor size, differentiation, TNM stage, and vascular invasion of primary liver cancer [17]. From data presented on these 72 cases published previously, the 4 specimens selected in the current study are representative of the others.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that SMC4-Homo-830 (Table 2) greatly decreased SMC4 expression [17]. SMC4-Homo-830 was cloned into Pgpu/GFP/ Neo-shNC vector (GenePharma, Shanghai, China), and transfected into 97-H and HepG2, HCC cell lines.…”

Section: Methodsmentioning

confidence: 99%

“…We further showed that expression of SMC4 may be useful for the early detection of HCC, and is related to the progression and invasion the tumor [17]. In the current study, we aimed to provide new insight into SMC4 function, and the mechanisms of growth and invasion of HCC.…”

Section: Introductionmentioning

confidence: 95%

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A novel miR-219-SMC4-JAK2/Stat3 regulatory pathway in human hepatocellular carcinoma

Zhou

Chen

Dong

et al. 2014

J Exp Clin Cancer Res

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BackgroundTo understand the involvement of structural maintenance of chromosome 4 (SMC4) in the development and progression of hepatocellular carcinoma (HCC).MethodsReal-time quantitative PCR and Western Blotting were applied to measure the expression of SMC4 in HCC samples and cell lines. The tumor-promoting effect of SMC4 was determined by WST-1, soft agar colony formation, cell motility and invasion assays. The SMC4 target signal pathway was identified by luciferase reporter and real-time quantitative PCR assays.ResultsThe upregulation of SMC4 was frequently detected in HCC samples and cell lines. Functional assays demonstrated that SMC4 could effectively promote tumor cell growth rate, colony formation in soft agar, wound-healing and invasion. Further studies showed that increased miR-219 levels caused a significant decrease in the SMC4 expression, and SMC4 inhibitor downregulated JAK2/Stat3 expression at both the mRNA and protein levels.ConclusionsOur findings provide new insight into SMC4 function and the mechanisms of growth and invasion of HCC.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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A novel miR-219-SMC4-JAK2/Stat3 regulatory pathway in human hepatocellular carcinoma

Zhou

Chen

Dong

et al. 2014

J Exp Clin Cancer Res

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“…C0105; Beyotime Institute of Biotechnology) was obtained from Beyotime Institute of Biotechnology. An immunohistochemical assay was performed on formalin-fixed, paraffin-embedded HCC tissues using antibodies against UBE2A (27). Briefly, 4 µm slides were deparaffinized through a series of xylene baths and graded alcohols.…”

Section: Hematoxylyin and Eosin (Hande) And Immunohistochemistrymentioning

confidence: 99%

High expression of ubiquitin-conjugating enzyme E2A predicts poor prognosis in hepatocellular carcinoma

Shen

et al. 2018

Oncol Lett

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Abstract. The present study aimed to illustrate the association of the expression of ubiquitin-conjugating enzyme E2A (UBE2A) with the clinicopathological parameters and prognosis in hepatocellular carcinoma (HCC). The expression levels of UBE2A mRNA and protein in a total of 276 HCC tissues and six liver cell lines was detected by fluorescent quantitative polymerase chain reaction, western blotting and immunohistochemistry. Statistical analysis was also performed to assess the association of the expression of UBE2A with the clinicopathological parameters and prognosis by the GraphPad Prism and SPSS version 21.0 software. UBE2A mRNA and protein were highly expressed in HCC tissues compared with those in the adjacent normal tissue. Immunohistochemical analysis revealed that UBE2A protein was more strongly stained in the 276 paraffin-embedded HCC tissues as compared with the 63 adjacent normal tissue. Statistical analysis also demonstrated that UBE2A expression was significantly associated with histological differentiation, TNM stage and vascular invasion of HCC (P<0.05). Notably, HCC patients with a high expression of UBE2A had a shorter survival time as compared with those with a low expression of UBE2A. There results suggested that UBE2A may be involved in the pathogenesis of HCC and may serve as an important prognostic marker.Further exploration of the involvement of UBE2A in HCC development may provide novel therapeutic targets. IntroductionHepatocellular carcinoma (HCC) is the third leading cause of cancer-associated mortality worldwide and the fifth most common cancer type (1). HCC is a global health burden and its prevalence varies worldwide (2). The incidence rate is reported to be higher in Asia (>20 cases/100,000 individuals) in comparison with that in North America and Europe (<5 cases/100,000 individuals) (3). The prognosis of HCC is poor, as evident by the fact that the number of annual mortality cases (~600,000) is almost equal to the number of new cases diagnosed annually (4). The median rate for 1-year survival is 80% (range, 63-97%), for 3-year survival is 70% (range, 34-78%) and for 5-year survival is 50% (range, 17-69%) (5). Surgery remains the most important treatment strategy for patients with HCC. The 5-year survival rate of patients with early HCC subsequent to resection treatment reaches 50%, although these patients exhibit a high recurrence rate (6,7). Despite advances in the diagnosis (8) and treatment (9) of HCC, the prognosis of this disease remains poor (10). Therefore, further clarification of the mechanisms underlying its development is important (11,12).At present, the prognosis of HCC is predicted based on imaging findings and biomarkers. Various biomarkers, including α-fetoprotein (AFP) (13), des-γ-ca rboxy prothrombin (14) and α-l-fucosidase (15), have been identified over the past three decades. However, accurate indicators for the prognosis of HCC are limited. Consequently, there is an urgency to develop a novel biomarker for the prognosis of HCC.The ubiquitin system serves a ...

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“…Other genes containing Tra2α/Tra2β target exons with G2 and S phase checkpoint that is essential in many cancer cells to prevent damaged chromosomes from entering mitosis [38] Vigilin (HDLBP) Represses proto-oncogene c-fms in breast cancer [43][44][45] KDM5A, KDM3A Histone methylases, erase epigenetic information, tumour promoters [46,47] NCOA Chromatin remodeling protein involved in breast cancer [48] ATRX Frequently mutated in paediatric cancer [49] SMC4 Key role in lung cancer, over-expressed in liver cancer [50,51] Nap1L1…”

Section: Tra2 Proteins Also Regulate Other Exons Potentially Importanmentioning

confidence: 99%

Transformer2 proteins protect breast cancer cells from accumulating replication stress by ensuring productive splicing of checkpoint kinase 1

Best

James

Hysenaj

et al. 2015

Front. Chem. Sci. Eng.

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Increased expression levels of the RNA splicing regulator Transformer2β (abbreviated Tra2β) have been reported in several types of cancer. Recent work has revealed an intimate cross-regulation between Tra2β and the highly similar Tra2α protein in human breast cancer cells, though these two proteins are encoded by separate genes created by a gene duplication that occurred over 500 million years ago. This cross-regulation involves splicing control of a special class of exons, called poison exons. Down-regulation of Tra2β reduces splicing inclusion of a poison exon in the mRNA encoding Tra2α, thereby up-regulating Tra2α protein expression. This buffers any splicing changes that might be caused by individual depletion of Tra2β alone. Discovery of this cross-regulation pathway, and its by-pass by joint depletion of both human Tra2 proteins, revealed Tra2 proteins are essential for breast cancer cell viability, and led to the identification of important targets for splicing control. These exons include a critical exon within the checkpoint kinase 1 (CHK1) gene that plays a crucial function in the protection of cancer cells from replication stress. Breast cancer cells depleted for Tra2 proteins have reduced CHK1 protein levels and accumulate DNA damage. These data suggest Tra2 proteins and/or their splicing targets as possible cancer drug targets.

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Overexpression of the structural maintenance of chromosome 4 protein is associated with tumor de-differentiation, advanced stage and vascular invasion of primary liver cancer

Cited by 48 publications

References 30 publications

A novel miR-219-SMC4-JAK2/Stat3 regulatory pathway in human hepatocellular carcinoma

A novel miR-219-SMC4-JAK2/Stat3 regulatory pathway in human hepatocellular carcinoma

High expression of ubiquitin-conjugating enzyme E2A predicts poor prognosis in hepatocellular carcinoma

Transformer2 proteins protect breast cancer cells from accumulating replication stress by ensuring productive splicing of checkpoint kinase 1

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