Impacts of Remifentanil on the Proliferation, Apoptosis, and Invasion of Esophageal Cancer Cells by Regulating Fas/FasL Signaling Pathway
LIU Sen1, XI Zhilong2, LI Liping1*
This study aims to investigate the impacts of remifentanil on the proliferation, apoptosis, and invasion of esophageal cancer cells, and to analyze whether its mechanism is related to the Fas (fatty acid synthase)/FasL (fatty acid synthase ligand) signaling pathway. Human esophageal cancer cells kyse30 were cultured in vitro and assigned into control group, remifentanil low, medium, and high concentration groups (10, 20, 40 nmol/L remifentanil), remifentanil high concentration+sh-NC group, and remifentanil high concentration+sh-Fas group. The cell morphology was observed under the transmission electron microscope. Cell viability, apoptosis, migration, invasion, and the expression of proteins related to Fas/FasL signaling pathway were detected using CCK-8 assay, flow cytometry, scratch assay, Transwell assay, and Western blot, respectively. The volume and mass of the transplanted tumors were detected by the nude mouse xenograft experiment. The results showed that the rough endoplasmic reticulum and mitochondria were abundant in the cytoplasm in the control group. In the remifentanil low, medium and high concentration groups, the cell volume shrank, the nucleus was concentrated and lysed, and multiple apoptotic bodies were formed. Compared with the control group, the remifentanil low, medium, and high concentration groups showed a decrease in cell D value, number of invasive cells, scratch healing rate, and Bcl- 2, PCNA, N-cadherin and Vimentin protein expression levels, and an raise in cell apoptosis rate, and Bax, Fas, and FasL protein expression levels (P<0.05). Compared with the remifentanil high concentration group and the remifentanil high concentration+sh-NC group, the remifentanil high concentration+sh-Fas group showed an raise in cell D value, scratchhealing rate, number of invasive cells, and PCNA, Bcl-2, Vimentin, N-cadherin protein expression levels, and a decrease in cell apoptosis rate, and Bax, Fas, and FasL protein expression levels (P<0.05). The tumor volume and mass in the remifentanil group were lower than those in the model group (P<0.05). The results indicate that remifentanil can inhibit the proliferation and invasion of esophageal cancer cells and induce their apoptosis. The mechanism may be related to the activation of the Fas/FasL signaling pathway.
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