Hao-Liang Zhao
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Hao-Liang Zhao has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Hongyan Jia
Department of Breast Surgery, First Hospital of Shanxi Medical University, China
1 shared publication Hui-Yu Li
1 shared publication- Huiyu Li
Department of General Surgery, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China
1 shared publication Jie Zhang
Department of General Surgery, The First Hospital of Shanxi Medical University, Taiyuan 030001, China
1 shared publicationJie-Feng He
1 shared publication- Shi-Ming Wang
First Hospital of Shanxi Medical University
1 shared publication
Latest Publications
- Open Access
- 16 July 2012
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 13 (7) , 8762-8774
MicroRNA-125b Functions as a Tumor Suppressor in Hepatocellular Carcinoma Cells
MicroRNAs (miRNAs) are important regulators of multiple cellular processes, and the deregulation of miRNA is a common event in diverse human diseases, particularly cancer. However, the mechanisms underlying the relationship between disordered miRNA expression and tumorigenesis have remained largely unknown. In this study, we demonstrated the down-regulation of miR-125b in hepatocellular carcinoma (HCC) tissues and HCC cell lines by Northern blot and quantitative RT-PCR analyses. The ectopic expression of miR-125b reduced the cellular proliferation and cell cycle progression of HCC cells by targeting Mcl-1 and IL6R. Furthermore, the miR-125b-induced inhibition of cell proliferation was rescued by the expression of Mcl-1 or IL6R variants that lacked 3' UTRs. Thus, this study revealed the differential expression of miR-125b in HCC cells and elucidated its potential as a tumor suppressor in HCC development.
- 16 July 2012
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 13 (7) , 8762-8774
Open AccessMicroRNA-125b Functions as a Tumor Suppressor in Hepatocellular Carcinoma Cells
MicroRNAs (miRNAs) are important regulators of multiple cellular processes, and the deregulation of miRNA is a common event in diverse human diseases, particularly cancer. However, the mechanisms underlying the relationship between disordered miRNA expression and tumorigenesis have remained largely unknown. In this study, we demonstrated the down-regulation of miR-125b in hepatocellular carcinoma (HCC) tissues and HCC cell lines by Northern blot and quantitative RT-PCR analyses. The ectopic expression of miR-125b reduced the cellular proliferation and cell cycle progression of HCC cells by targeting Mcl-1 and IL6R. Furthermore, the miR-125b-induced inhibition of cell proliferation was rescued by the expression of Mcl-1 or IL6R variants that lacked 3' UTRs. Thus, this study revealed the differential expression of miR-125b in HCC cells and elucidated its potential as a tumor suppressor in HCC development.
- 1 February 2012
- Vol. 34 (1) , 58-61
[Inhibitory effect of NSC348884, a small molecular inhibitor of nucleophosmin, on the growth of hepatocellular carcinoma cell line hepG2].
To investigate the effect of NSC348884, a nucleophosmin small molecular inhibitor, on the growth of hepatocellular carcinoma cell line HepG2 and its underlying mechanism. After HepG2 cells were treated by NSC348884 for 4 days, the effect of HepG2 cells on proliferation was measured by methyl thiazolyl tetrazolium (MTT) assay, the expression variation of nucleophosmin oligomer and monomer was measured using Western blotting, and cell apoptotic rate was detected by flow cytometry. The proliferation of HepG2 cells was remarkably inhibited by NSC348884 treatment when the drug concentration ranged from 1 micromol/L to 10 micromol/L (P < 0.05), with a 50% inhibiting concentration of 1.4 micromol/L. After treatment for 24 hours, the expression level of nucleophosmin oligomer decreased obviously while that of nucleophosmin monomer increased (both P < 0.05). After treatment by 1 micromol/L and 2 micromol/L NSC348884, the 24-hour apoptotic rates of HepG2 cells were (13.770 +/- 0.335)% and (19.021 +/- 0.237)%, respectively, which were significantly higher than in the control group (6.950 +/- 0.207)% (P < 0. 05). NSC348884 can promote the transformation of nucleophosmin oligomer to monomer and thus inhibit the growth of hepatic carcinoma cell line HepG2 in vitro.
- 1 February 2012
- Vol. 34 (1) , 58-61
[Inhibitory effect of NSC348884, a small molecular inhibitor of nucleophosmin, on the growth of hepatocellular carcinoma cell line hepG2].
To investigate the effect of NSC348884, a nucleophosmin small molecular inhibitor, on the growth of hepatocellular carcinoma cell line HepG2 and its underlying mechanism. After HepG2 cells were treated by NSC348884 for 4 days, the effect of HepG2 cells on proliferation was measured by methyl thiazolyl tetrazolium (MTT) assay, the expression variation of nucleophosmin oligomer and monomer was measured using Western blotting, and cell apoptotic rate was detected by flow cytometry. The proliferation of HepG2 cells was remarkably inhibited by NSC348884 treatment when the drug concentration ranged from 1 micromol/L to 10 micromol/L (P < 0.05), with a 50% inhibiting concentration of 1.4 micromol/L. After treatment for 24 hours, the expression level of nucleophosmin oligomer decreased obviously while that of nucleophosmin monomer increased (both P < 0.05). After treatment by 1 micromol/L and 2 micromol/L NSC348884, the 24-hour apoptotic rates of HepG2 cells were (13.770 +/- 0.335)% and (19.021 +/- 0.237)%, respectively, which were significantly higher than in the control group (6.950 +/- 0.207)% (P < 0. 05). NSC348884 can promote the transformation of nucleophosmin oligomer to monomer and thus inhibit the growth of hepatic carcinoma cell line HepG2 in vitro.