CircRNA02318 Exerts Therapeutic Effects on Myocardial Ischemia-Reperfusion Injury Rats by Regulating the Nox1/Akt Through Inhibiting Drebrin

We investigated the role of circ_0132269 in hepatocellular carcinoma (HCC). We examined circ_0132269 levels in HCC tissues and cell lines using qRT-PCR. Survival analysis was performed to assess the correlation between circ_0132269 expression and HCC patient survival rates. Knockdown of circ_0132269 was performed to evaluate its impact on HCC cell proliferation, migration, and invasion. Bioinformatics analysis predicted that circ_0132269 could interact with miR-1248. This interaction was confirmed using dual luciferase assays, and the correlation between circ_0132269 and miR-1248 was analyzed. Further functional experiments investigated the effect of miR-1248 on circ_0132269-mediated malignant phenotypes. circ_0132269 was significantly upregulated in HCC tissues and cell lines. Higher circ_0132269 expression correlated with poorer overall and disease-free survival in HCC patients. Silencing circ_0132269 suppressed HCC cell proliferation, migration, and invasion. Bioinformatics analysis revealed a binding site between circ_0132269 and miR-1248. miR-1248 expression was reduced in HCC, while its target MTO1 was highly expressed. miR-1248 levels showed a negative correlation with circ_0132269 and MTO1 levels, while circ_0132269 and MTO1 exhibited a positive correlation. Overexpression of miR-1248 partially reversed the promotive effect of highly expressed circ_0132269 on HCC cell behaviors. circ_0132269 was significantly upregulated in HCC and associated with poor prognosis. It interacts with miR-1248 to regulate HCC malignancy, highlighting its potential as a diagnostic and therapeutic target.

Effects of Circ_0132269 on the Progression of Hepatocellular Carcinoma via Targeting miR-1248/MTO1

Yu,

Hu,

Wang

et al. 2023

The Role and Mechanism of circAMOTL1 in Hypertensive Heart Failure

Mou,

Fan,

Sun

et al. 2024

To explore the changes of circAMOTL1 expression, cell function and expression of fibrosis-related proteins in myocardial hypertrophy and fibrosis model. Human cardiomyocytes AC16 were cultured, and the concentration of Ang II was firstly explored by CCK-8. After determining the optimal dose of Ang II, AC16 cells were induced to construct an in vitro model of myocardial hypertrophy and fibrosis. CCK-8 was utilized to assess cell proliferation. Flow cytometry was performed to validate cell cycle and apoptosis. circAMOTL1, miR-330-3p, smad7, Col1a2 and Col3a1 genes expressions were assessed by qRT-PCR. smad7, Col1a2 and Col3a1 proteins expressions were evaluated using Western blot and IF. FISH was performed to detect circAMOTL1 localization in cells. 10 μM Ang II was selected for subsequent experiments. Compared with control group, cell viability of the Ang II group was significantly decreased, apoptosis was observably increased, circAMOTL1 and smad7 expressions were signally repressed, miR-330-3p, Col1a2 and Col3a1 expressions were notably increased. Both circAMOTL1 and miR-330-3p, miR-330-3p and smad7 had targeted binding sites. Overexpression of circAMOTL1 promoted AC16 cells proliferation and inhibited apoptosis. In addition, overexpression of circAMOTL1 inhibited miR-330-3p and promoted smad7 expression. Overexpression of circAMOTL1 inhibited miR-330-3p and promoted smad7 expression. circAMOTL1 may be a potential target for treating hypertensive heart failure.

The Role of miRNA-29b1 on the Hypoxia-Induced Apoptosis in Mammalian Cardiomyocytes

Liu,

Juan,

et al. 2024

A hypoxic stress which causes apoptosis of cardiomyocytes is the main problem in the ischemic heart disease. The present research sought to investigate the role of microRNA-29b1 (miR-29b1) in hypoxia-treated cardiomyocytes and its potential mechanism involved. We replicated an in vitro AC16 and H9C2 cardiomyocytes ischemia model by hypoxia (1% O2, 48 h) treatment. Cell apoptosis was evaluated by flow cytometry using Annexin V FITC-PI staining assay. Moreover, we used western blot and immunofluorescence analysis to determine the expression of Bcl-2, Bax caspase-3 and Cx43 proteins. We found that miR-29b1 protected AC16 and H9C2 cells from hypoxia-induced injury as the evidences that miR-29b1 attenuated the effects of hypoxia treatment on AC16 and H9C2 cell apoptosis after hypoxia treatment. In conclusion, these results revealed the potential cardiovascular protective effects of miR-29b1 in the process of ischemia-related myocardial injury.