Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway

• Z.M. Bai ^[1] ; X.F. Li ^[2] ; Y. Yang ^[3] ; Y.F. Yang ^[4] ; D.R. Lv ^[1] ; L.L. Tang ^[1]
  1. [1] Department of Anesthesiology, Wuwei People’s Hospital, North Side of Xuanwu Street, Liangzhou District, Wuwei 733000, China
  2. [2] Department of Neonatology, Wuwei People’s Hospital, Wuwei 733000, China
  3. [3] Department of Chinese Medicine, Rheumatology and Immunology, Wuwei Liangzhou Hospital, Wuwei 733000, China
  4. [4] Department of Neurocardiology, Wuwei Second People’s Hospital, Wuwei 733000, China

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• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 23, Nº. 9, 2021, págs. 1866-1873
• Idioma: inglés
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• Resumen

  • Purpose The aim of the present study was to elucidate the functional role of hsa-miR-328-3p/STAT3 pathway in the effects of propofol on gastric cancer proliferation.

    Methods Bioinformatics was used to analyze the molecular expression differences of hsa-miR-328-3p/STAT3 axis in stom- ach adenocarcinoma (n = 435) and normal samples (n = 41) from TCGA database. The expression of the above molecules in gastric cancer cells SGC-7901 and normal gastric mucosal cells GES-1 was verified via qPCR. The dual-luciferase assay was carried out to confirm the interaction between hsa-miR-328-3p and STAT3. Subsequently, the cell proliferation and the expression of the above molecules in SGC-7901 and GES-1 cells were evaluated after 10 μM propofol treatment. Finally, we analyzed whether propofol still inhibited the proliferation of gastric cancer by suppressing STAT3 pathway after hsa- miR-328-3p down-regulation.

    Results Compared with normal samples, the expression of hsa-miR-328-3p was significantly down-regulated in stomach adenocarcinoma samples, while the expression of STAT3 and downstream target genes (MMP2, CCND1 and COX2) was up-regulated. The results were consistent with those in GES-1 and SGC-7901 cell lines. Meanwhile, we found that hsa- miR-328-3p can bind to the 3′-UTR of the potential target gene STAT3. Furthermore, propofol significantly inhibited the proliferation of gastric cancer cell line SGC-7901, where hsa-miR-328-3p was up-regulated and the expression of STAT3 and downstream proliferation-related target genes were down-regulated. However, the growth inhibition of propofol on SGC-7901 cell was significantly reversed after the inhibition of hsa-miR-328-3p.

    Conclusions To sum up, propofol suppressed the STAT3 pathway via up-regulating hsa-miR-328-3p to inhibit gastric cancer proliferation.