scholarly journals Expression and Significance of MicroRNA-183 in Hepatocellular Carcinoma

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Zenghui Liang ◽  
Yingtang Gao ◽  
Wenxia Shi ◽  
Daokuan Zhai ◽  
Shilei Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Diseases ◽  
Area Under The Curve ◽  
Chronic Viral Hepatitis ◽  
Kaplan Meier ◽  
Viral Hepatitis B ◽  
Clinicopathologic Factors ◽  
Polymerase Chain ◽  
Benign Liver ◽  
Normal Controls

Objective. In our previous study, we found that some miRNAs were deregulated in hepatocellular carcinoma (HCC), including miR-183. However, the expression of miR-183 in the progression of benign liver diseases to HCC and its correlation with clinicopathologic factors remain undefined.Methods. MiR-183 expression was measured in normal controls (NC) (n=21), chronic viral hepatitis B or C (CH) tissues (n=10), liver cirrhosis (LC) tissues (n=18), HCC tissues (n=92), and adjacent nontumor tissues (NT) (n=92) by quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR).Results. The expression levels of miR-183 were significantly higher in HCC than in NT, LC, CH, and NL (P=0.001,P<0.001,P=0.011,P<0.001, resp.). The upregulated miR-183 in HCC was correlated with TNM stage (P=0.042) and cirrhosis (P=0.025). The Kaplan-Meier survival analysis showed that miR-183 expression was not associated with the survival of HCC patients. However, miR-183 yielded an area under the curve (AUC) of 0.808 with 59.8% sensitivity and 91.8% specificity in discriminating HCC from benign liver diseases (CH and LC) or NC.Conclusions. The upregulated miR-183 may associate with onset and progression of HCC, but not with the patient survival. A further research is needed to determine the potential of miR-183 as biomarker for HCC.

Thrombopoietin levels in serum and liver tissue in patients with chronic viral hepatitis and hepatocellular carcinoma

2000 ◽  
Vol 99 (3) ◽  
pp. 207-214 ◽  
Author(s):  
Michiko OKUBO ◽  
Goshi SHIOTA ◽  
Hironaka KAWASAKI
Keyword(s):  
Hepatocellular Carcinoma ◽  
Viral Hepatitis ◽  
Liver Diseases ◽  
Total Mass ◽  
Sandwich Elisa ◽  
Chronic Viral Hepatitis ◽  
Rt Pcr ◽  
Platelet Counts ◽  
Indocyanine Green Test ◽  
Normal Controls

Thrombocytopenia in liver diseases is considered to be due to splenic platelet pooling and accelerated destruction. Since thrombopoietin (TPO), a regulator of thrombopoiesis, is produced mainly in the liver, decreased production of TPO may account for thrombocytopenia in liver diseases. To address this issue, we measured serum TPO, using a sensitive sandwich ELISA, in 108 patients with chronic viral hepatitis, which included chronic hepatitis (CH) and liver cirrhosis (LC), and hepatocellular carcinoma (HCC), and in 29 normal controls. TPO mRNA in 78 liver samples was examined by reverse transcription (RT)-PCR. Platelet counts in CH, LC, HCC and controls were 176±15×109/l, 81±8×109/l, 99±7×109/l and 234±9×109/l respectively. Serum TPO levels in CH, LC and HCC were 2.79±0.4 fmol/ml, 1.49±0.2 fmol/ml and 1.97±0.2 fmol/ml, and were higher than those of controls. Serum TPO levels were positively correlated with prothrombin time and serum albumin (P < 0.05, in each case), and negatively correlated with Indocyanine Green test and Pugh score (P < 0.01 and P < 0.05 respectively). However, RT-PCR and immunohistochemistry showed that expression of TPO mRNA and protein were similar in the different liver diseases, suggesting that serum TPO is a reflection of the total mass of functional liver. Platelet counts were negatively correlated with spleen index, but not with serum TPO. These results suggest that thrombocytopenia in liver disease is not directly associated with serum TPO but is associated with hypersplenism.

scholarly journals Downregulated Expression of linc-ROR in Gastric Cancer and Its Potential Diagnostic and Prognosis Value

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Xiuchong Yu ◽  
Haixiang Ding ◽  
Yijiu Shi ◽  
Liangwei Yang ◽  
Jiaming Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Noncoding Rna ◽  
Area Under The Curve ◽  
Diagnostic Value ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Polymerase Chain ◽  
Long Intergenic Noncoding Rna ◽  
Clinical Potential ◽  
The Relationship

Background. Gastric cancer (GC) is one of the global mortality diseases and has a poor prognosis due to the lack of ideal tumor biomarkers. Numerous studies have shown that long noncoding RNAs (lncRNAs) can affect the occurrence and development of cancer through a variety of signaling pathways. The abnormal expression and specificity of lncRNAs in tumors make them potential biomarkers of cancers. Nevertheless, the diagnostic roles of lncRNAs in GC have been poorly understood. So this study focuses on the clinical diagnostic value of lncRNAs in GC. Materials and Methods. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to investigate the expression of the linc-ROR (long intergenic noncoding RNA, regulator of reprogramming) in 105 paired GC tissues and adjacent normal tissues. Receiver operating characteristic (ROC) curve and area under the curve (AUC) were established to assess the diagnostic value of linc-ROR. The relationship between expression of linc-ROR and clinicopathological factors of patients with GC was further explored. Kaplan-Meier analysis was performed to evaluate the prognostic value of linc-ROR expression. Results. The linc-ROR expression level was significantly decreased in GC tissues compared with its adjacent nontumor tissues ( n = 105 , P < 0.001 ). We also discovered that linc-ROR was evidently downregulated in 68.6% (72/105) of GC tissues. The AUC’s value of linc-ROR was up to 0.6495, with sensitivity and specificity of 0.7524 and 0.5143, respectively. Intriguingly, the linc-ROR expression levels were obviously associated with tumor differentiation ( P = 0.004 ). Notably, the overall survival rate of GC patients with high expression of linc-ROR was significantly higher than those with low expression. Conclusion. Our data revealed that linc-ROR has clinical potential as a biomarker for the diagnosis of GC and assessment of its prognosis.

scholarly journals Oxidative Stress Management in Chronic Liver Diseases and Hepatocellular Carcinoma

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1576 ◽  
Author(s):  
Daisuke Uchida ◽  
Akinobu Takaki ◽  
Atsushi Oyama ◽  
Takuya Adachi ◽  
Nozomu Wada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Viral Hepatitis ◽  
Liver Diseases ◽  
Chronic Viral Hepatitis ◽  
Chronic Liver ◽  
Chronic Liver Diseases ◽  
Anti Cancer ◽  
The Impact

Chronic viral hepatitis B and C and non-alcoholic fatty liver disease (NAFLD) have been widely acknowledged to be the leading causes of liver cirrhosis and hepatocellular carcinoma. As anti-viral treatment progresses, the impact of NAFLD is increasing. NAFLD can coexist with chronic viral hepatitis and exacerbate its progression. Oxidative stress has been recognized as a chronic liver disease progression-related and cancer-initiating stress response. However, there are still many unresolved issues concerning oxidative stress, such as the correlation between the natural history of the disease and promising treatment protocols. Recent findings indicate that oxidative stress is also an anti-cancer response that is necessary to kill cancer cells. Oxidative stress might therefore be a cancer-initiating response that should be down regulated in the pre-cancerous stage in patients with risk factors for cancer, while it is an anti-cancer cell response that should not be down regulated in the post-cancerous stage, especially in patients using anti-cancer agents. Antioxidant nutrients should be administered carefully according to the patients’ disease status. In this review, we will highlight these paradoxical effects of oxidative stress in chronic liver diseases, pre- and post-carcinogenesis.

scholarly journals ITGB1 Drives Hepatocellular Carcinoma Progression by Modulating Cell Cycle Process Through PXN/YWHAZ/AKT Pathways

2021 ◽  
Vol 9 ◽  
Author(s):  
Jinghe Xie ◽  
Tingting Guo ◽  
Zhiyong Zhong ◽  
Ning Wang ◽  
Yan Liang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Bioinformatics Analysis ◽  
Cycle Progression ◽  
Migration Assay ◽  
Normal Tissues ◽  
Polymerase Chain ◽  
Interfering Rna ◽  
Normal Controls

Integrin β1 (ITGB1), which acts as an extracellular matrix (ECM) receptor, has gained increasing attention as a therapeutic target for the treatment of hepatocellular carcinoma (HCC). However, the underpinning mechanism of how ITGB1 drives HCC progression remains elusive. In this study, we first found that ITGB1 expression was significantly higher in HCC tissues than in normal controls by bioinformatics analysis. Furthermore, bioinformatics analysis revealed that paxillin (PXN) and 14-3-3 protein zeta (YWHAZ) are the molecules participating in ITGB1-regulated HCC tumor cell cycle progression. Indeed, immunohistochemistry (IHC) revealed that ITGB1, paxillin, and YWHAZ were strongly upregulated in paired HCC tissue compared with adjacent normal tissues. Notably, the inhibition of ITGB1 expression by small interfering RNA (siRNA) resulted in the downregulated expression of PXN and YWHAZ in primary HCC cells, as assessed by western blot and immunostaining. In addition, ITGB1 knockdown markedly impaired the aggressive behavior of HCC tumor cells and delayed cell cycle progression as determined by cell migration assay, drug-resistance analysis, colony formation assay, quantitative real-time polymerase chain reaction (qRT-PCR), and cell cycle analysis as well as cell viability measurements. More importantly, we proved that xenograft ITGB1high tumors grew more rapidly than ITGB1low tumors. Altogether, our study showed that the ITGB1/PXN/YWHAZ/protein kinase B (AKT) axis enhances HCC progression by accelerating the cell cycle process, which offers a promising approach to halt HCC tumor growth.

Gradually increased Golgi protein 73 expression in the progression of benign liver diseases to precancerous lesions and hepatocellular carcinoma correlates with prognosis of patients

2013 ◽  
Vol 43 (11) ◽  
pp. 1199-1210 ◽  
Author(s):  
Shi-Gang Shan ◽  
Ying-Tang Gao ◽  
Yan-Jie Xu ◽  
Yong Huang ◽  
Qin Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Diseases ◽  
Precancerous Lesions ◽  
Golgi Protein ◽  
Benign Liver

scholarly journals Decreased serum exosomal miR-320a expression is an unfavorable prognostic factor in patients with hepatocellular carcinoma

2020 ◽  
Vol 48 (4) ◽  
pp. 030006051989614
Author(s):  
Xinjie Hao ◽  
Ruopei Xin ◽  
Wenjing Dong
Keyword(s):  
Hepatocellular Carcinoma ◽  
Operating Characteristic ◽  
Characteristic Curve ◽  
Diagnostic Value ◽  
Positive Lymph Node ◽  
Circulating Micrornas ◽  
Independent Prognostic Marker ◽  
Potential Biomarker ◽  
Polymerase Chain ◽  
Normal Controls

Objective Circulating microRNAs (miRNAs) have promising potential as diagnostic or prognostic biomarkers for hepatocellular carcinoma (HCC). This study aimed to analyze the clinical significance of serum exosomal miR-320a expression in patients with HCC. Methods A total of 104 patients with HCC, 55 patients with chronic liver disease (CLD), and 50 healthy volunteers were enrolled. Serum exosomal miR-320a levels were measured by quantitative reverse-transcriptase polymerase chain reaction and compared among the groups. The relationships between exosomal miR-320a levels and clinicopathological factors in patients with HCC were also analyzed. Results Serum exosomal miR-320a levels were significantly lower in patients with HCC compared with patients with CLD and healthy controls. Receiver-operating characteristic curve analysis showed that serum exosomal miR-320a had good diagnostic value for distinguishing between HCC subjects and normal controls. Serum exosomal miR-320a levels were significantly elevated 1 month after surgery in patients with HCC. Moreover, serum exosomal miR-320a downregulation was strongly associated with positive lymph node metastasis, positive vein invasion, advanced TNM stage, and shorter survival. Serum exosomal miR-320a was confirmed as an independent prognostic marker for HCC. Conclusions Collectively, these results indicate that serum exosomal miR-320a might be a potential biomarker for the detection and prognosis of HCC.

Correlation of prognosis with the gradually increased Golgi protein 73 expression in the progression of benign liver diseases to precancerous lesions and hepatocellular carcinoma.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e15050-e15050
Author(s):  
Yijun Wang ◽  
Shigang Shan ◽  
Yingtang Gao ◽  
Qin Zhang ◽  
Fengmei Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Prognostic Factor ◽  
Liver Diseases ◽  
Precancerous Lesions ◽  
Disease Free Survival ◽  
Low Grade ◽  
Mrna Levels ◽  
Group B ◽  
High Level ◽  
Benign Liver

e15050 Background: Serum golgi protein73 (sGP73) is a novel biomarker for hepatocellular carcinoma (HCC). However, there are few reports on the pattern of GP73 expression in the progression of benign liver diseases to precancerous lesions and HCC. This study aimed to investigate GP73 expression and it correlation with clinicopathologic parameters. Methods: Tissue GP73 (tGP73) levels were detected in specimens of group A (n=186) including HCC (n=62), peritumoral tissue (PTL) (n=43), high/low-grade hepatic atypical hyperplasia (AH) (n=32/2), chronic hepatitis B (CHB) (n=42) and normal controls (NC) (n=5) by immunohistochemistry, and GP73 expression in group B (n=159) and group C (n=16) were detected by RT-PCR and Western blot respectively. sGP73 levels were detected in subjects of group D (n=287) by ELISA. Results: GP73 expression increased gradually from NC, CHB, PTL to high-grade AH and HCC at both protein and mRNA levels (P<0.05), while sGP73 in HCC group was lower than in liver cirrhosis (LC) group (P<0.001). Both tGP73 and sGP73 levels were negatively associated with tumor size and TNM stage, and tGP73 levels were positively associated with tumor differentiation. The high-tGP73 group showed significantly better overall and disease-free survival than low-tGP73 group (P=0.008, P=0.018). Multivariate analysis revealed that the tGP73 level was an independent prognostic factor for HCC, but not sGP73. Conclusions: GP73 increases gradually in the progression ofbenign liver diseases to precancerous lesions and HCC. This expression pattern suggests the regulatory mechanism of GP73 is related to the progression of chronic liver diseases. Furthermore, a high level of tGP73 is a favorable prognostic factor for HCC.

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