Combined evaluation of centromere protein H and Ki-67 as prognostic biomarker for patients with gastric carcinoma

He, Weiling; Li, Y.H.; Yang, Dajun; Wu, Song; Chen, X.L.; Liu, F.K.; Wang, Z.; Li, W.; Chen, W.; Chen, C.Y.; He, Yulong; Zhan, Wen Hua

doi:10.1016/j.ejso.2012.08.023

Cited by 34 publications

(34 citation statements)

References 26 publications

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“…Compared with the control cells, the population doubling time was shorter and the colony formation ability was decreased in Tca8113/CENP-H RNAi cells, which highlighted the compromised viability caused by the downregulation of CENP-H (18). Consistent with these studies (12,17,18), our MTT and colony formation data also revealed that shRNA-mediated CENP-H knockdown caused Hep3B proliferation inhibition. Similarly to the in vitro experiments, Lv3-CENP-H1 cells exhibited decreased tumorigenicity in nude mice in vivo.…”

Section: Discussionsupporting

confidence: 78%

“…Survivin, a member of the inhibitor of apoptosis protein family, has been implicated as a protector against cell apoptosis; the aberrant high expression of this factor in cancers is closely correlated with advanced disease and poor overall survival (20,21). According to previous studies, CENP-H siRNA decreases the protein expression of survivin, indicating apoptosis induction (12,18). Wang et al (22) found that siRNA knockdown of CENP-H mRNA promoted FaDu cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…Centromere protein-H (CENP-H), a fundamental component of the human active centromere complex (8), has been found to be upregulated in human colorectal cancer, and the ectopic expression of CENP-H induces aneuploidy (9). Recently, accumulating evidence revealed that the abnormal expression of CENP-H is closely associated with several cancers including esophageal (10) and gastric carcinoma (11,12), breast (13) and uterine cervical cancer (14).…”

Section: Introductionmentioning

confidence: 99%

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CENP-H regulates the cell growth of human hepatocellular carcinoma cells through the mitochondrial apoptotic pathway

Hou

et al. 2017

Oncology Reports

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Abstract. The genomic alterations of hepatocellular carcinoma (HCC) are still unclear. Centromere protein-H (CENP-H) has been shown to be associated with many solid tumors. Our previous study found that CENP-H was upregulated in HCC and was related to patient prognosis. However, the biological functions of CENP-H in HCC and the possible underlying mechanisms have not been well elucidated. In the present study, we demonstrated that CENP-H knockdown inhibited the proliferation of Hep3B cells and decreased colony formation ability of single cells in vitro. Furthermore, CENP-H knockdown induced Hep3B cell apoptosis, and apoptotic bodies were observed using transmission electron microscopy. The protein expression of cleaved caspase-3 was upregulated in Hep3B cells after CENP-H knockdown. Additionally, a Bax/Bcl-2 ratio imbalance with a significant increase of Bax and a substantial decrease of Bcl-2 at both the mRNA and protein levels were determined in this study. In an animal experiment, CENP-H knockdown blocked the growth of Hep3B subcutaneous xenografts. Immunohistochemistry revealed that the protein expression of cleaved caspase-3 and Bax was increased, whereas the protein expression of Bcl-2 and Ki-67 was decreased in subcutaneous xenografts of the CENP-H-knockdown group. In summary, CENP-H may be involved in cell proliferation and apoptosis of HCC cells through the mitochondrial apoptotic pathway. Combined with previous studies, the data provide a new perspective on HCC development and progression.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CENP-H regulates the cell growth of human hepatocellular carcinoma cells through the mitochondrial apoptotic pathway

Hou

et al. 2017

Oncology Reports

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“…Procedures were in accordance with previous protocols [23]. Cells cultured in chamber slides (Thermo Fisher Scientific, Waltham, MA, United States) were washed, fixed, and permeabilized.…”

Section: Methodsmentioning

confidence: 99%

Anti-Fibrotic Effects of Astragaloside IV in Systemic Sclerosis

Mao

et al. 2014

Cell Physiol Biochem

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Objective: To evaluate the anti-fibrotic effects of Astragaloside IV in systemic sclerosis. Methods: Treated or untreated systemic sclerosis (SSc) and normal fibroblast isolated from corresponding pairs were utilized to detect expression of collagen and fibronectin by western blot, quantitative real-time RT-PCR (RT-qPCR), immunofluorescence staining and histopathological examination. SSc mouse model induced by bleomycin was used to evaluate the effects of the drug in vivo. Results: Compared to normal fibroblast (NF), the expression of collagen and fibronectin in SSc (SScF) dramatically increased, and this could be reduced by Astragaloside IV (AST) in a dose- or time-dependent manner at both protein and mRNA levels. Administration of Astragaloside IV consistently decreased collagen formation and partially restored the structure, as well as suppressing collagen and fibronectin expression in the skin lesions of SSc-model mice. Mechanistically, Astragaloside IV-induced fibrosis reduction may be due to deregulation of Smad 3/Fli-1, the major mediators of the fibrotic response and key molecules for TGF-β signaling. Astragaloside IV also decreased the level of p-SMAD3 and completely blocked its relocation into the nuclei. Conclusion: Astragaloside IV attenuates fibrosis by inhibiting the TGF-β-Smads3 axis in systemic sclerosis.

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“…The included data were extracted from each of the eligible studies (7,9,10,(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31): the first author's name, year of publication, study location, antibody manufacturer, dilution ratio of Ki-67 or MIB-1 antibody, cutoff value for high Ki-67 LI, number of patients analyzed, and pathological tumor-node-metastasis (pTNM) stage. For quantitative aggregation of survival results, the correlation between high Ki-67 LI and overall or disease-free survival rate was analyzed according to the hazard ratio (HR) using 1 of 3 methods.…”

Section: Data Extractionmentioning

confidence: 99%

Meta-Analysis of Prognostic Role of Ki-67 Labeling Index in Gastric Carcinoma

Pyo

Kim

2017

Int J Biol Markers

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Background This meta-analysis aimed to elucidate the prognostic role of the Ki-67 labeling index (LI) in gastric cancer (GC). Methods The current study included 3,615 GC patients in 20 eligible studies, and evaluated the prognostic role of Ki-67 LI in GC. Subgroup analysis was conducted based on depth of invasion and cutoff value for high Ki-67 LI. Results A high Ki-67 LI correlated significantly with worse survival (hazard ratio [HR] = 1.214, 95% confidence interval [CI], 1.004-1.468). However, there was no significant correlation between high Ki-67 LI and worse survival in advanced GC (HR = 1.252, 95% CI, 0.801-1.956). The subgroup with cutoff value ≤25% showed a significant correlation with worse survival, but this was not seen in the subgroup with cutoff >25% (HR = 1.433, 95% CI, 1.094-1.876 vs. HR = 1.005, 95% CI, 0.801-1.262). In addition, in the 10% < Ki-67 LI ≤ 20% range, there was a significant correlation between high Ki-67 LI and worse overall survival (HR = 1.931, 95% CI, 1.013-3.310). Conclusions A high Ki-67 LI correlated significantly with a worse prognosis in GC patients. Further cumulative studies for the optimal cutoff value for high Ki-67 LI are needed before application in clinical practice.

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Combined evaluation of centromere protein H and Ki-67 as prognostic biomarker for patients with gastric carcinoma

Cited by 34 publications

References 26 publications

CENP-H regulates the cell growth of human hepatocellular carcinoma cells through the mitochondrial apoptotic pathway

CENP-H regulates the cell growth of human hepatocellular carcinoma cells through the mitochondrial apoptotic pathway

Anti-Fibrotic Effects of Astragaloside IV in Systemic Sclerosis

Meta-Analysis of Prognostic Role of Ki-67 Labeling Index in Gastric Carcinoma

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