OBJECTIVE: To explore the influence of exosome-derived micro-ribonucleic acid (miR)-21 on chemotherapy resistance of esophageal cancer and its mechanism. MATERIALS AND METHODS: Human esophageal cancer TE-1 and Eca109/DDP cell lines and human normal esophageal Het-1A cells were cultured, and the exosomes were extracted from cells. After miR-21 was inhibited with an inhibitor and overexpressed with miRNA mimics combined with cisplatin, the cell viability was detected via cell counting kit-8 (CCK-8), the interaction between miR-21 and programmed cell death 4 (PDCD4) was detected via dual-luciferase reporter gene assay, and the changes in the protein level were detected via Western blotting. RESULTS: The expression level of exosome-derived miR-21 in esophageal cancer cells was higher than that in normal esophageal cells, and it was the highest in cisplatin-resistant esophageal cancer cells. After treatment with cisplatin, miR-21 overexpression significantly reduced the invasion ability of esophageal cancer cells. After miR-21 overexpression, the sensitivity of esophageal cancer cells to cisplatin was lowered. MiR-21 interacted with the 3'-untranslated region (UTR) of PDCD4. Moreover, the miR-21 overexpression significantly down-regulated the mRNA and protein levels of PDCD4 in cells. CONCLUSIONS: MiR-21 affects the sensitivity of esophageal cancer to cisplatin through targeting PDCD4.
OBJECTIVE: To explore the influence of exosome-derived micro-ribonucleic acid (miR)-21 on chemotherapy resistance of esophageal cancer and its mechanism. MATERIALS AND METHODS:Humanesophageal cancer TE-1 and Eca109/DDP cell lines and human normal esophageal Het-1A cells were cultured, and the exosomes were extracted from cells. After miR-21 was inhibited with an inhibitor and overexpressed with miRNA mimics combined with cisplatin, the cell viability was detected via cell counting kit-8 (CCK-8), the interaction between miR-21 and programmed cell death 4 (PDCD4) was detected via dual-luciferase reporter gene assay, and the changes in the protein level were detected via Western blotting. RESULTS: The expression level of exosome-derived miR-21 in esophageal cancer cells was higher than that in normal esophageal cells, and it was the highest in cisplatin-resistant esophageal cancer cells. After treatment with cisplatin, miR-21 overexpression significantly reduced the invasion ability of esophageal cancer cells. After miR-21 overexpression, the sensitivity of esophageal cancer cells to cisplatin was lowered. MiR-21 interacted with the 3'-untranslated region (UTR) of PDCD4. Moreover, the miR-21 overexpression significantly down-regulated the mRNA and protein levels of PDCD4 in cells. CONCLUSIONS:MiR-21 affects the sensitivity of esophageal cancer to cisplatin through targeting PDCD4.