scholarly journals MCM10 Acts as a Potential Prognostic Biomarker and Promotes Cell Proliferation in Hepatocellular Carcinoma: Integrated Bioinformatics Analysis and Experimental Validation

2020 ◽  
Vol Volume 12 ◽  
pp. 9609-9619
Author(s):  
Wei Wan ◽  
Yu Shen ◽  
Quanxi Li
2021 ◽  
Author(s):  
Nanni Hua ◽  
Chen Yang ◽  
Anxian Chen ◽  
Yi Feng ◽  
Xianglei He ◽  
...  

Abstract Background ConclusionsFibrinogen-like protein-1 (FGL1), as the member of FREP superfamily, had been widely concerned as a major immune inhibitory ligand of LAG-3. Although FGL1 expression levels didn’t have significant difference in most of tumors via online data analysis, we found that it was down-regulated in liver cancer. Moreover, the correlation between FGL1 expression and the progression and prognosis of hepatocellular carcinoma (HCC) was still disputed. Methods In our study, firstly, we used bioinformatics analysis to define the expression profile and clinical significance of FGL1 in HCC. Then, we determined the FGL1 level in human HCC cell lines, tumor and normal liver tissues from HCC patients by western blot. Furthermore, tissue microassays were used to detect the expression of FGL1 through immunohistochemistry staining and verify whether FGL1 expression levels were associated with clinicopathological features of HCC patients. Results The results proved that FGL1 was down-regulated significantly in HCC cell lines and HCC tissues, corresponding with the results of our bioinformatics analysis. FGL1 expression levels in HCC were related to Edmondson grade and metastasis. Additionally, high FGL1 expression was related to better overall survival in HCC patients, indicating that the down-regulated FGL1 was correlated with poor prognosis and FGL1 might function as a tumor suppressor. Conclusions Taken together, expression levels of FGL1 may correlate with the progression and prognosis of HCC, and FGL1 could be a potential prognostic biomarker.


Gene ◽  
2019 ◽  
Vol 698 ◽  
pp. 9-18 ◽  
Author(s):  
Chuanfei Li ◽  
Di Zhou ◽  
Xiaoling Jiang ◽  
Minhui Liu ◽  
Hui Tang ◽  
...  

2021 ◽  
Author(s):  
Nanni Hua ◽  
Anxian Chen ◽  
Chen Yang ◽  
Hui Dong ◽  
Xianglei He ◽  
...  

Abstract Fibrinogen-like protein-1 (FGL1), as the member of FREP superfamily, had been widely concerned as a major immune inhibitory ligand of LAG-3. Although FGL1 expression levels didn’t have significant difference in most of tumors via online data analysis, we found that it was down-regulated in liver cancer. Moreover, the correlation between FGL1 expression and the progression and prognosis of hepatocellular carcinoma (HCC) was still disputed. In our study, firstly, we used bioinformatics analysis to define the expression profile and clinical significance of FGL1 in HCC. Then, we determined the FGL1 level in 9 human HCC cell lines and 11 pairs of tumor and normal liver tissues from HCC patients by western blot. Furthermore, tissue microassays were used to detect the expression of FGL1 through immunohistochemistry staining and verify whether FGL1 expression levels were associated with clinicopathological features of HCC patients or not. The results of the experiment proved that FGL1 was down-regulated significantly in HCC cell lines and HCC tissues, corresponding with the results of our bioinformatics analysis. FGL1 expression levels in HCC were related to Edmondson grade and metastasis. Additionally, high FGL1 expression was related to better overall survival in HCC patients, indicating that the down-regulated FGL1 was correlated with poor prognosis and FGL1 might function as a tumor suppressor. Taken together, expression levels of FGL1 may correlate with the progression and prognosis of HCC, and FGL1 could be a potential prognostic biomarker.


Author(s):  
Guangying Cui ◽  
Huifen Wang ◽  
Wenli Liu ◽  
Jiyuan Xing ◽  
Wengang Song ◽  
...  

Glycogen metabolism plays a key role in tumorigenesis. High expression levels of glycogen phosphorylase B (PYGB) were reported in several cancers and might be served as a prognostic biomarker for cancer from precancerous lesions. Previous studies indicated the high expression of PYGB in hepatocellular carcinoma (HCC) tissues. However, the detailed roles of PYGB in HCC, as well as the regulatory mechanisms, are still unclear. In this study, we confirmed that PYGB was overexpressed in HCC tissues. PYGB overexpression was significantly associated with an aggressive tumor phenotype and poor prognosis of HCC patients. Functionally, PYGB knockdown suppressed HCC cell proliferation, migration and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Bioinformatics analysis indicated that PYGB overexpression might enhance epithelial to mesenchymal transition (EMT) in HCC. Moreover, miR-101-3p was identified to post-transcriptionally inhibit the expression of PYGB via binding to 3′-UTR of PYGB. Overexpression of PYGB antagonized the regulatory effect of miR-101-3p on cell proliferation, migration and invasion in HCC cells. In summary, our results suggest that miR-101-3p/PYGB axis has an important role in HCC and PYGB could be served as a novel prognostic biomarker and therapeutic target for improving the prognosis of HCC patients.


2021 ◽  
pp. 1-7
Author(s):  
Rady Eid El-Araby ◽  
Rabab S. Hamad ◽  
Najla K. Al Abdulsalam ◽  
Ahmed R. Mashaal ◽  
Rady Eid El-Araby

Hepatocellular carcinoma (HCC) remains the main type of liver cancer. Understanding the molecular and immune mechanisms of HCC tumorigenesis are required to develop effective biomarkers. This study is designed to measure the circulating MMP9 and CEBPα to provide a diagnostic and prognostic biomarker for HCV-genotype (4) induced liver cirrhosis and carcinogenesis. This study included one hundred Egyptian patients, divided into two groups 50 patients each. The first group: classified into Chronic Liver Disease (CLD) without cirrhosis (n=25) and CLD with cirrhosis (n=25). The second group: classified into CLD patients with HCC, (n=25), and healthy control (25 volunteers). The expression of MMP9 and CEBPα genes were analysed using Real-Time PCR. Our results showed significant downregulation in MMP9 and CEBPα genes in cirrhotic and HCC patients (p< 0.001 and p<0.001) respectively. There was a significant (p< 0.001) diagnostic capacity between HCC patients against CLD with or without cirrhosis patients. Bioinformatics analysis revealed a relationship between MMP9 and CEBPα genes. In conclusion, the gradual decrease in the expression of MMP9 and CEBPα gene during the progression of the disease recommended use of MMP9 and CEBPα genes as a diagnostic and prognostic biomarker for both cirrhosis and HCC in HCV-genotype (4) patients.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Min Hu ◽  
Yaowu Han ◽  
Ying Zhang ◽  
Yuanfeng Zhou ◽  
Lin Ye

Abstract Background Our preliminary bioinformatics analysis showed that lncRNA TINCR may absorb miR-214-5p by serving is sponge, while miR-214-5p targets ROCK1. This study aimed to investigate the interactions among these 3 factors in hepatocellular carcinoma (HCC). Methods Expression of TINCR, ROCK1 and miR-214-5p in HCC and non-tumor tissues was detected by performing qPCR. The correlations among TINCR, ROCK1 and miR-214-5p in HCC tissues were analyzed by performing linear regression. Overexpression experiments were performed to analyze gene interactions. Cell proliferation was analyzed by CCK-8 assay. Results We found that TINCR and ROCK1 were upregulated, while miR-214-5p was downregulated in HCC. TINCR and ROCK1 were positively correlated, while TINCR and miR-214-5p were not significantly correlated. In HCC cells, TINCR overexpression is followed by ROCK1 overexpression, while miR-214-5p overexpression induced the downregulation of ROCK1. In addition, TINCR and miR-214-5p did not affect the expression of each other. TINCR and ROCK1 overexpression led to increased rate of cancer cell proliferation, while miR-214-5p played an opposite role and reduced the effects of TINCR overexpression. Therefore, TINCR sponges miR-214-5p to upregulate ROCK1 in HCC, thereby promoting cancer cell invasion and migration.


2001 ◽  
Vol 71 (3) ◽  
pp. 116-125
Author(s):  
Norina Basa ◽  
Daniela Lazar ◽  
Remus Cornea ◽  
Sorina Taban ◽  
Melania Ardelean ◽  
...  

Alteration of β-catenin expression is involved in the development and evolution of hepatocellular carcinoma (HCC); β-catenin is able to influence tumor cell proliferation. We analyzed the immunohistochemical (IHC) expression of β-catenin on a group of 32 patients diagnosed with HCC using the anti-β-catenin monoclonal antibody (clone E247). We correlated the expression of β-catenin with the proliferation index of Ki-67 (PI Ki-67), the mitotic index (MI) and other clinical and pathological features. We observed an altered β-catenin expression in 58.38% of all HCC cases. This expression was insignificantly correlated with tumor size (]5 cm) (p = 0.683), histological grade G1-G2 (p = 0.307), vascular invasion (p = 0.299) and advanced pT stage (p = 0.453); we obtained a significantly higher MI in HCC with altered β-catenin expression (p = 0.018), as compared to HCC without overexpression (1.66 � 1.37) (p = 0.038) and a PI Ki-67 of 22.49 � 20.1 and 28.24 � 18.2, respectively in tumors with altered β-catenin expression with insignificant differences compared to HCC without overexpression (25.95 � 15.2) (p = 0.682 and p = 0.731, respectively). According to the results we obtained, aberrant β-catenin expression in HCC was correlated with a high mitotic index, therefore playing an important role in tumor progression by stimulating tumor cell proliferation; non-nuclear β-catenin overexpression can have a pathological significance in HCC, especially in cases of HCC associated with hepatitis B virus (HBV) infection.


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