<p>Lung cancer is the leading cause of cancer-related deaths worldwide, with a high mortality rate due to late-stage diagnosis and limited treatment options. Interleukin-1 alpha (IL-1α) is an inflammatory signalling cytokine that promotes tumour cell growth and proliferation. It is released as a damage-associated molecular pattern (DAMP) molecule in response to cell injury and inflammation. However, the role of IL-1α in lung cancer is not addressed enough. This study aims to investigate the modulatory effects of IL-1α in lung cancer. We examined the impact of IL-1α on lung cancer cell growth and viability using the MTT assay. A549 lung cancer lines were treated with different concentrations of human recombinant IL-1α (0.1 ng/mL, 1.0 ng/mL, 10 ng/mL, 100ng/mL). The regulation of pro-tumorigenic gene expression including interleukin-8 (IL-8), C-X-C motif chemokine ligand 1 (CXCL1) and matrix metalloproteinase 7 (MMP7) was analysed using RT-qPCR. The results demonstrated an increase in the percentage of cell viability with increasing IL-1α concentration relative to the control. The gene expression of MMP7 was upregulated, while CXCL1 and IL-8 showed trends toward upregulation without reaching statistical significance. Overall, these findings suggest that IL-1α modulates lung cancer cell growth and the expression of genes associated with pro-tumorigenic pathways highlighting its potential role in tumour progression and supporting further investigation of IL-1α-mediated mechanisms.</p>

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Modulatory Effects of Interleukin 1-alpha (IL-1α) in Lung Cancer Cell Line A549

  • Zaridatul Aini Ibrahim,
  • Shazura Izleen Abd Rahim,
  • Suha Azizan,
  • Zher Pin Goh,
  • Farid Nazer Faruqu

摘要

Lung cancer is the leading cause of cancer-related deaths worldwide, with a high mortality rate due to late-stage diagnosis and limited treatment options. Interleukin-1 alpha (IL-1α) is an inflammatory signalling cytokine that promotes tumour cell growth and proliferation. It is released as a damage-associated molecular pattern (DAMP) molecule in response to cell injury and inflammation. However, the role of IL-1α in lung cancer is not addressed enough. This study aims to investigate the modulatory effects of IL-1α in lung cancer. We examined the impact of IL-1α on lung cancer cell growth and viability using the MTT assay. A549 lung cancer lines were treated with different concentrations of human recombinant IL-1α (0.1 ng/mL, 1.0 ng/mL, 10 ng/mL, 100ng/mL). The regulation of pro-tumorigenic gene expression including interleukin-8 (IL-8), C-X-C motif chemokine ligand 1 (CXCL1) and matrix metalloproteinase 7 (MMP7) was analysed using RT-qPCR. The results demonstrated an increase in the percentage of cell viability with increasing IL-1α concentration relative to the control. The gene expression of MMP7 was upregulated, while CXCL1 and IL-8 showed trends toward upregulation without reaching statistical significance. Overall, these findings suggest that IL-1α modulates lung cancer cell growth and the expression of genes associated with pro-tumorigenic pathways highlighting its potential role in tumour progression and supporting further investigation of IL-1α-mediated mechanisms.