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Background <p>The process of cancer progression is maintained through a feedback loop whereby reactive oxygen species (ROS) induce inflammatory cytokines, which activate STAT3 and result in miRNA-21 upregulation. miRNA-21 enhances the AKT signaling pathway and suppresses PTEN, promoting the proliferation of the cancerous cells and the additional production of ROS. Neupogen exerts both anti-inflammatory oxidant effects, our previous study revealed the anticancer effect of neupogean on colorectal adenocarcinoma cells, thus we aimed to investigate the possible modulating role of Neupogen on tumor microenvironment by breaking the inflammatory cytokine-STAT3-miRNA21 loop.</p> Methods <p>Hep2 cells were cultured in four conditions (1) untreated Hep2 cells, (2) Hep2 cells treated with Neupogen, (3) Hep2 cells treated with MSCs-conditioned media, and (4) Hep2 cells treated with both MSCs-conditioned media and Neupogen. MTT assay was used to assess cell proliferation, ROS levels was assessed by ELISA, STAT3 protein expression was assessed by western blotting technique, and qRT-PCR was used to assess the gene expression of IL-6, TNF-alpha, VEGF, and miRNA-21.</p> Results <p>Neupogen or MSCs-conditioned media treatment significantly decreased the ROS accumulation, STAT3 expression, pro-inflammatory cytokines, miRNA-21 levels, and cell proliferation. The combination treatment generated the highest inhibitory effects in all measured parameters.</p> Conclusion <p>Neupogen and MSCs-conditioned media are effective in suppressing the proliferation of Hep2 cells by targeting various components of the ROS-cytokine- STAT3-miRNA-21 signaling axis. Their combined therapy has shown potent anticancer effects, which are promising to be used in multi-targeted cancer treatment.</p> Graphical abstract <p></p>

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Neupogen/MSCs conditioned media inhibit HEp-2 laryngeal cancer cells proliferation by down regulating miRNA 21expression and ROS production

  • 期刊论文

  • 发表日期：

    2026年6月24日

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  • Abeer Mostafa,
  • Heba M. Amr,
  • Naglaa F. Abozeid,
  • Mona Mohamed Ahmed,
  • Mohamed Hassan Gad,
  • Inas Harb,
  • Noha Samir Abdel Latif,
  • Azza Abusree Ahmed

摘要

Background

The process of cancer progression is maintained through a feedback loop whereby reactive oxygen species (ROS) induce inflammatory cytokines, which activate STAT3 and result in miRNA-21 upregulation. miRNA-21 enhances the AKT signaling pathway and suppresses PTEN, promoting the proliferation of the cancerous cells and the additional production of ROS. Neupogen exerts both anti-inflammatory oxidant effects, our previous study revealed the anticancer effect of neupogean on colorectal adenocarcinoma cells, thus we aimed to investigate the possible modulating role of Neupogen on tumor microenvironment by breaking the inflammatory cytokine-STAT3-miRNA21 loop.

Methods

Hep2 cells were cultured in four conditions (1) untreated Hep2 cells, (2) Hep2 cells treated with Neupogen, (3) Hep2 cells treated with MSCs-conditioned media, and (4) Hep2 cells treated with both MSCs-conditioned media and Neupogen. MTT assay was used to assess cell proliferation, ROS levels was assessed by ELISA, STAT3 protein expression was assessed by western blotting technique, and qRT-PCR was used to assess the gene expression of IL-6, TNF-alpha, VEGF, and miRNA-21.

Results

Neupogen or MSCs-conditioned media treatment significantly decreased the ROS accumulation, STAT3 expression, pro-inflammatory cytokines, miRNA-21 levels, and cell proliferation. The combination treatment generated the highest inhibitory effects in all measured parameters.

Conclusion

Neupogen and MSCs-conditioned media are effective in suppressing the proliferation of Hep2 cells by targeting various components of the ROS-cytokine- STAT3-miRNA-21 signaling axis. Their combined therapy has shown potent anticancer effects, which are promising to be used in multi-targeted cancer treatment.

Graphical abstract