| Title | AngII induces HepG2 cells to activate epithelial-mesenchymal transition |
| Authors | Qi, Minghua Zhou, Yuanping Liu, Jikui Ou, Xi Li, Minghua Long, Xia Ye, Jing Yu, Guangyin |
| Affiliation | Beijing Univ, Shenzhen Hosp, Dept Infect Dis, 1120 Lianhua Rd, Shenzhen 518035, Guangdong, Peoples R China. Southern Med Univ, Nanfang Hosp, Dept Infect Dis, 1838 Guangzhou Dadao Rd, Guangzhou 510515, Guangdong, Peoples R China. Beijing Univ, Shenzhen Hosp, Dept Infect Dis, 1120 Lianhua Rd, Shenzhen 518035, Guangdong, Peoples R China. Zhou, YP (reprint author), Southern Med Univ, Nanfang Hosp, Dept Infect Dis, 1838 Guangzhou Dadao Rd, Guangzhou 510515, Guangdong, Peoples R China. |
| Keywords | angiotensin II hepatocellular carcinoma epithelial-mesenchymal transition RENIN-ANGIOTENSIN SYSTEM II TYPE-1 RECEPTOR LONG-TERM USE HEPATOCELLULAR-CARCINOMA BREAST-CANCER GROWTH RISK ADENOCARCINOMA ANGIOGENESIS EXPRESSION |
| Issue Date | 2018 |
| Publisher | EXPERIMENTAL AND THERAPEUTIC MEDICINE |
| Citation | EXPERIMENTAL AND THERAPEUTIC MEDICINE. 2018, 16(4), 3471-3477. |
| Abstract | The present study aimed to determine whether HepG2 can induce epithelial-mesenchymal transition (EMT) via angiotensin II (AngII) simulation. The expression levels of EMT markers vimentin and E-cadherin in cancer tissues and adjacent tissues of patients with hepatocellular carcinoma (HCC) were detected by immunohistochemistry. In addition, HepG2 cells were stimulated with AngII, and the gene and protein expression levels of vimentin and E-cadherin were measured by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively, whereas cell migration and invasion were assessed using Transwell assays. The AngII inhibitor Ang1-7 and the Ang1-7 inhibitor A779 were added to the system to further evaluate AngII-induced EMT. Compared with that in normal tissue, the expression level of vimentin in HCC tissue was increased, whereas that of E-cadherin was decreased. EMT occurred 48 h following AngII stimulation. The transcription level of E-cadherin in HepG2 cells was decreased, whereas that of vimentin was increased. In addition, the migration and invasion abilities of the cells were increased simultaneously. Ang1-7 partly inhibited AngII-induced EMT. When stimulated at an appropriate time, HepG2 cells have the ability to undergo EMT. |
| URI | http://hdl.handle.net/20.500.11897/522833 |
| ISSN | 1792-0981 |
| DOI | 10.3892/etm.2018.6610 |
| Indexed | SCI(E) |
| Appears in Collections: | 深圳医院 |
