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Propofol inhibited gastric cancer proliferation via the hsa-miR-328-3p/STAT3 pathway
Bai, Z. M; Lv, D. R; Tang, L. L; Li, X. F; Yang, Y; Yang, Y. F.
Afiliación
  • Bai, Z. M; Wuwei People’s Hospital. Department of Anesthesiology. Liangzhou District. China
  • Lv, D. R; Wuwei People’s Hospital. Department of Anesthesiology. Liangzhou District. China
  • Tang, L. L; Wuwei People’s Hospital. Department of Anesthesiology. Liangzhou District. China
  • Li, X. F; Wuwei People’s Hospital. Department of Neonatology. Wuwei. China
  • Yang, Y; Wuwei Liangzhou Hospital. Rheumatology and Immunology. Department of Chinese Medicine. Wuwei. China
  • Yang, Y. F; Wuwei Second People’s Hospital. Department of Neurocardiology. Wuwei. China
Clin. transl. oncol. (Print) ; Clin. transl. oncol. (Print);23(9): 1866-1873, sept. 2021. ilus, graf
Article en En | IBECS | ID: ibc-222186
Biblioteca responsable: ES1.1
Ubicación: ES15.1 - BNCS
ABSTRACT
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 stomach 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 (AU)
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Colección: 06-national / ES Base de datos: IBECS Asunto principal: Neoplasias Gástricas / Adenocarcinoma / Propofol / MicroARNs / Proliferación Celular / Factor de Transcripción STAT3 Límite: Humans Idioma: En Revista: Clin. transl. oncol. (Print) Año: 2021 Tipo del documento: Article
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Colección: 06-national / ES Base de datos: IBECS Asunto principal: Neoplasias Gástricas / Adenocarcinoma / Propofol / MicroARNs / Proliferación Celular / Factor de Transcripción STAT3 Límite: Humans Idioma: En Revista: Clin. transl. oncol. (Print) Año: 2021 Tipo del documento: Article