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| Impact of miR-145-5p-Mediated Regulation of Survivin via the Apoptotic Pathway on the Biological Behavior of Esophageal Cancer |
| ZHENG Jingxiong, et al |
| The Affiliated Hospital of Chengde Medical University, Hebei Chengde 067000, China |
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Abstract Objective: To explore the impact of miR-145-5p targeting Survivin and the apoptotic signaling pathway on apoptosis, invasion, and migration in esophageal cancer.Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to detect the relative expression levels of miR-145-5p and Survivin mRNA in esophageal cancer tissues and cell lines. A dual-luciferase reporter gene analysis was conducted to validate the targeted regulatory relationship between miR-145-5p and Survivin. RT-qPCR was used to measure the relative expression levels of miR-145-5p and Survivin mRNA after cell transfection. Western blot was performed to assess the expression of BCL2, MDM2, and Caspase-3 proteins in the apoptotic pathway. Cell survival, apoptosis rate, migration rate, and invasion ability were evaluated using MTT, flow cytometry, scratch healing, and Transwell chamber experiments in TE-1 cells. Results: Compared to adjacent normal tissues, miR-145-5p was downregulated, while Survivin was upregulated in cancer tissues (P<0.05). In comparison to normal esophageal mucosal epithelial HEEC cells, TE-1 cells exhibited low expression of miR-145-5p and high expression of Survivin (P<0.05). Dual-luciferase reporter gene experiments confirmed the targeted regulatory relationship between miR-145-5p and Survivin. Transfection with miR-145-5p mimic significantly increased miR-145-5p expression, inhibited Survivin mRNA expression, downregulated BCL2 and MDM2 protein expression, upregulated Caspase-3 expression, promoted cell apoptosis, and inhibited cell viability, invasion, and migration compared to untransfected and miR-145-5p control-transfected TE-1 cells (P<0.05). Conclusion: Through negative regulation by miR-145-5p, the expression of Survivin is inhibited, leading to the activation of the apoptotic pathway. This promotes cell apoptosis and inhibits the survival, invasion, and migration capabilities of esophageal cancer cells.
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2024, Vol. 30 
