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Cytokine‑driven positive feedback loop organizes fibroblast transformation and facilitates gastric cancer progression

  • Xian-Kui Cao [1] ; Bin Xie [1] ; Yang Shao [1] ; Jie Lin [1]
    1. [1] Department of General Surgery, Liaoning Province Cancer Hospital and Institute (Cancer Hospital of China Medical University), No. 44 Xiaoheyan Road, Dadong District, Shenyang 110042, Liaoning, China
  • Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 24, Nº. 7, 2022, págs. 1354-1364
  • Idioma: inglés
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  • Resumen
    • ackground Gastric cancer (GC) is a malignancy that belongs to one of the most common leading causes of cancer death.

      Cancer-associated fibroblasts (CAFs) promote the GC cells’ malignant behavior. It is still unknown how GC converts normal fibroblasts (NFs) to CAFs.

      Methods GC cells were co-cultured with NFs. Bioinformatics was used to analyze the genes and signaling pathways that were changed in fibroblast. RT-PCR, western blot, and Elisa assays were used to detect the expression of cytokines in fibroblast and condition medium. Western blot and immunofluorescence demonstrated activation of relevant pathways in CAFs-like cells. Transwell, scrape, colony formation, and CCK-8 assays were performed to reveal the feedback effect of CAFs-like cells on GC cells.

      Results GC promoted the conversion of NFs to CAFs by secreting Interleukin 17A (IL-17). It included both morphological and molecular marker changes. This process was achieved by activating the nuclear factor-κB (NF-κB) pathway. On the other hand, CAFs cells could secrete C-X-C Motif Chemokine Ligand 8 (IL-8, IL-8), which promoted the malignant phenotype of GC cells. In this way, a feedback loop of mutual influence was constructed in the GC and tumor microenvironment (TME).

      Conclusions Our research proved a novel model of GC-educated NFs. GC-IL-17-fibroblast-IL-8-GC axis might be a potential pathway of the interaction between GC and TME.


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