Dysregulation of serum microRNA-574-3p and its clinical significance in hepatocellular carcinoma

Author(s):  
Xianjuan Shen ◽  
Yajing Xue ◽  
Hui Cong ◽  
Xudong Wang ◽  
Shaoqing Ju

Objectives To explore microRNA-574-3p expression in serum of patients with hepatocellular carcinoma and investigate correlations between serum microRNA-574-3p expression and the development and prognosis of hepatocellular carcinoma. Design and methods Serum samples were collected from 70 patients with primary hepatocellular carcinoma, 40 patients with cirrhosis and 45 healthy controls. Serum microRNA-574-3p expression levels were detected by real-time quantitative polymerase chain reaction. The linearity, specificity and reproducibility were evaluated. In addition, the diagnostic value of microRNA-574-3p and its correlations with clinicopathologic features were assessed. Results The relative expression of microRNA-574-3p in hepatocellular carcinoma patients, cirrhosis patients and healthy controls was 2.306 (1.801–3.130), 1.362 (0.994–1.665) and 1.263 (0.765–1.723), respectively, indicating that it was significantly higher in hepatocellular carcinoma patients than that in the other two groups ( U = 439.5, 514.5, both P < 0.0001) and was significantly correlated with hepatitis B virus DNA copies ( U = 383.0, P = 0.018). In hepatitis B virus-positive hepatocellular carcinoma patients, the relative expression of microRNA-574-3p was significantly correlated with hepatitis B virus DNA concentration ( r = 0.348, P = 0.022). Compared with healthy control group, AUCROC of serum microRNA-574-3p in hepatocellular carcinoma group was 0.837 with 95% CI: 0.763–0.910. Combining microRNA-574-3p, AFU and alpha-fetoprotein together, the sensitivity was highest compared with other markers alone or combined. Conclusions The relative expression of serum microRNA-574-3p in hepatocellular carcinoma patients was significantly higher than that in cirrhosis patients and healthy controls, and it may be an important biomarker in the auxiliary diagnosis of hepatocellular carcinoma.

1986 ◽  
Vol 17 (2) ◽  
pp. 202-204 ◽  
Author(s):  
Tomoyuki Tnaka ◽  
Hiroyuki Miyamoto ◽  
Okio Hino ◽  
Tomoyuki Kitagawa ◽  
Michio Koike ◽  
...  

1978 ◽  
Vol 2 (3) ◽  
pp. 207-214 ◽  
Author(s):  
Jesse Summers ◽  
Anna O'Connell ◽  
Philippe Maupas ◽  
Alain Goudeau ◽  
Pierre Coursaget ◽  
...  

2021 ◽  
Author(s):  
Hiroaki Kanzaki ◽  
Tetsuhiro Chiba ◽  
Tatsuya Kaneko ◽  
Junjie Ao ◽  
Na Qiang ◽  
...  

Abstract Previous RNA immunoprecipitation followed by proteomic approaches successfully demonstrated that Embryonic Lethal, Abnormal Vision, Drosophila-Like 1 (ELAVL1) interacts with hepatitis B virus (HBV)-derived RNAs. Although ELAVL family proteins stabilize AU-rich element (ARE)-containing mRNAs, their role in HBV transcription remains unclear. This study conducted loss-of-function assays of ELAVL1 for inducible HBV-replicating HepAD38 cells and HBx-overexpressed HepG2 cells. In addition, clinicopathological analyses in primary hepatocellular carcinoma (HCC) surgical samples have also been conducted. Lentivirus-mediated short hairpin RNA knockdown of ELAVL1 resulted in a decrease in both viral RNA transcription and production of viral proteins, including HBs and HBx. Cell growth in tetracycline-treated replication-stopping HepAD38 cells was more significantly impaired in ELAVL1 knockdown than those in the control group, indicating that ELAVL1 is involved in proliferation not only by the suppression of HBV replication but also by other factors. Immunohistochemical analyses of 77 paired HCC surgical specimens have demonstrated that diffuse ELAVL1 expression was detected more frequently in HCC tissues (61.0%) than in nontumor tissues (27.3%). In addition, the abundant expression of ELAVL1 tended to affect postoperative recurrence in HBV-related HCC patients. In conclusion, ELAVL1 contributes not only to HBV replication but also to HCC cell growth. It may be a potent therapeutic target for HBV-related HCC treatment.


1988 ◽  
Vol 62 (3) ◽  
pp. 861-865 ◽  
Author(s):  
F Imazeki ◽  
K Yaginuma ◽  
M Omata ◽  
K Okuda ◽  
M Kobayashi ◽  
...  

Cancer ◽  
1986 ◽  
Vol 58 (5) ◽  
pp. 1055-1060 ◽  
Author(s):  
Fumio Imazeki ◽  
Masao Omata ◽  
Osamu Yokosuka ◽  
Kunio Okuda

1983 ◽  
Vol 11 (2) ◽  
pp. 99-104 ◽  
Author(s):  
Whan Kook Chung ◽  
Hee Sik Sun ◽  
Doo Ho Park ◽  
Gerald Y. Minuk ◽  
Jay H. Hoofnagle

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