Open Access

Dexmedetomidine hydrochloride plus sufentanil citrate inhibits glucose metabolism and epithelial‑mesenchymal transition in human esophageal squamous carcinoma KYSE30 cells by modulating the JAK/STAT3/HIF‑1α axis

  • Authors:
    • Weijing Li
    • Yong Wang
    • Xiaolin Li
    • Han Wu
    • Li Jia
  • View Affiliations

  • Published online on: April 18, 2024     https://doi.org/10.3892/ol.2024.14406
  • Article Number: 273
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Dexmedetomidine hydrochloride (DEX‑HCl) and sufentanil citrate (SFC) are commonly used anesthetic drugs for esophageal cancer (EC) surgery. The present study was performed to investigate the effect of DEX‑HCl and SFC treatment on glucose metabolism and epithelial‑mesenchymal transition in EC. Cell counting kit‑8 (CCK8), clonogenic, wound healing and Transwell migration assays were performed to assess the effects of the DEX‑HCl and SFC on KYSE30 cell proliferation, invasion and migration. Changes in lactate and glucose levels in KYSE30 cells were also detected. Western blot analysis was used to determine the protein expression levels of the JAK/STAT signaling pathway and glucose metabolism‑related proteins. The results of CCK8, clonogenic and wound healing assays demonstrated that DEX‑HCl and SFC inhibited KYSE30 cell proliferation, invasion and migration. Similarly, the combined DEX‑HCl and SFC treatment significantly reduced lactate production, ATP production and glucose levels in KYSE30 cells. Western blotting indicated that DEX‑HCl and SFC could reduce JAK/STAT and metastasis‑related protein expression. Demonstrating a reduction in Hexokinase 2, matrix metallopeptidase 2 and 9, N‑cadherin and lactate dehydrogenase A protein expression levels. The effects of DEX‑HCl and SFC combined treatment were counteracted by the addition of JAK/STAT pathway activator RO8191, which suggested that DEX‑HCl and SFC could serve a role in mediating the JAK/STAT signaling pathway in KYSE30 cells.
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June-2024
Volume 27 Issue 6

Print ISSN: 1792-1074
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Spandidos Publications style
Li W, Wang Y, Li X, Wu H and Jia L: Dexmedetomidine hydrochloride plus sufentanil citrate inhibits glucose metabolism and epithelial‑mesenchymal transition in human esophageal squamous carcinoma KYSE30 cells by modulating the JAK/STAT3/HIF‑1α axis. Oncol Lett 27: 273, 2024
APA
Li, W., Wang, Y., Li, X., Wu, H., & Jia, L. (2024). Dexmedetomidine hydrochloride plus sufentanil citrate inhibits glucose metabolism and epithelial‑mesenchymal transition in human esophageal squamous carcinoma KYSE30 cells by modulating the JAK/STAT3/HIF‑1α axis. Oncology Letters, 27, 273. https://doi.org/10.3892/ol.2024.14406
MLA
Li, W., Wang, Y., Li, X., Wu, H., Jia, L."Dexmedetomidine hydrochloride plus sufentanil citrate inhibits glucose metabolism and epithelial‑mesenchymal transition in human esophageal squamous carcinoma KYSE30 cells by modulating the JAK/STAT3/HIF‑1α axis". Oncology Letters 27.6 (2024): 273.
Chicago
Li, W., Wang, Y., Li, X., Wu, H., Jia, L."Dexmedetomidine hydrochloride plus sufentanil citrate inhibits glucose metabolism and epithelial‑mesenchymal transition in human esophageal squamous carcinoma KYSE30 cells by modulating the JAK/STAT3/HIF‑1α axis". Oncology Letters 27, no. 6 (2024): 273. https://doi.org/10.3892/ol.2024.14406