RESUMEN
@#[Abstract] Objective: To investigate the effects of long non-coding RNA zinc finger antisense 1 (lncRNA ZFAS1) on the proliferation, invasion, and migration of liver cancer cells by regulating the miR-588/high mobility group AT-hook protein 2 (HMGA2) axis. Methods: Real-time fluorescent quantitative PCR (qRT-PCR) and western blot were performed to measure the expression levels of ZFAS1, miR-588 and HMGA2 in 80 pairs of liver cancer tissues and corresponding para-cancerous issues (the tissue sample were collected from Shouyi Campus, Wuhan Third Hospital during Jan. 2018 and Dec. 2019), human normal liver cell line (LO2) and liver cancer cell lines (HepG2, Huh7, HCCLM3). The survival of patients was analyzed using the Kaplan-Meier survival curve. HepG2 cells were divided into blank group, si-NC group, si-ZFAS1 group, si-ZFAS1+inhibitor NC group, and si-ZFAS1+miR-588 inhibitor group. qPCR was performed to measure the expression of ZFAS1 and miR-588 in HepG2 cells of each group, and Western blot was performed to measure the expression of HMGA2 protein in the cells. CCK-8 method, Transwell, and scratch test were performed to measure the proliferation, invasion, and migration of HepG2 cells. Dual-luciferase reporter gene experiment was performed to verify the targeting relationship between ZFAS1 and miR-588 as well as between miR-588 and HMGA2. A HepG2 cell transplanted tumor model was established in nude mice to examine the effect of silencing ZFAS1 or/and miR-588 on the growth of transplanted tumors. Results: ZFAS1 and HMGA2 were highly expressed while miR-588 was lowly expressed in liver cancer tissues and liver cancer cells (all P<0.05). The 2-year survival rate of patients with low ZFAS1 expression was higher than that in the high expression group (P<0.05). Compared with the blank group, the relative expression of ZFAS1 and HMGA2 protein in the si-ZFAS1 group was significantly reduced, and the relative expression of miR-588 was significantly increased (all P<0.05); compared with the si-ZFAS1 group, the relative expression of ZFAS1 in the si-ZFAS1+miR-588 inhibitor group did not change significantly (P>0.05), however, the relative expression of HMGA2 protein was significantly increased, and the relative expression of miR-588 was significantly reduced (P<0.05). Silencing ZFAS1 was able to inhibit the proliferation, invasion, and migration of HepG2 cells and inhibit the growth of transplanted tumors in nude mice (all P<0.05). ZFAS1 targeted and down-regulated the expression of miR-588, while miR-588 targeted and down-regulated the expression of HMGA2. Simultaneous inhibition of miR-588 expression could reverse the inhibitory effects of silencing ZFAS1 on the proliferation, invasion, and migration of HepG2 cells and the growth of transplanted tumors in nude mice (all P<0.05). Conclusion: Silencing ZFAS1 may down-regulate the expression of HMGA2 by promoting the expression of miR-588, thereby inhibiting the proliferation, invasion, and migration of liver cancer HepG2 cells.
RESUMEN
Objective:To explore the effects and molecular mechanism of circ_001598 on biological behavior of breast cancer (BC) cells.Methods:Sevoflurane in different concentrations were used to treat BC cells and the cell activity and apoptosis were detected. qRT-PCR was used to determine the relative expression of Circ_001598 and miR-588 in BC tissue and cells. The effects of Sevoflurane on Circ_001598, miR-588 expression was detected. Dual luciferase reporter gene assay was used to detect the relationship between Circ_001598 and miR-588. The expression of Circ_001598, miR-588 in BC cells was intervened, then cell activity and apoptosis level was detected by using MTT and flow cytometry individually.Results:Sevoflurane inhibited cell activity of BC cells, and promoted cell apoptosis. Circ_001598 was increased in BC tissue and cells, but Sevoflurane could down-regulate the expression of Circ_001598 (all P<0.05) . Overexpression of Circ_001589 partially saved the effects of Sevoflurane on cell viability and apoptosis. Circ_001598 negatively regulated miR-588 in BC cells. miR-588 expression was down-regulated in BC tissue and cells, but Sevoflurane up-regulated the expression level of miR-588 in BC cells (all P<0.05) . miR-588 transfection partially offseted the effects of Circ_001598 on Sevoflurane induced BC cells apoptosis. Conclusion:Sevoflurane affects BC cell viability and apoptosis via regulating Circ_001589/miR-588.