Avicenna Research Institute Avicenna Journal of Medical Biotechnology 2008-2835 18 3 2026 08 01 miR-103/107–Mediated Suppression of NKILA Enhances Oncogenic Behaviors in Human Lung Cancer Cells 216 222 250464 10.18502/ajmb.v18i3.22238 EN Davood Jafari Department of Immunology, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran Hossein Naghiloo Student Research Committee, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran Seyyed Shamsadin Athari Department of Immunology, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran Farshid Noorbakhsh Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Nima Rezaei Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran Journal Article 2025 11 29 Background: Lung cancer remains a major global health burden, and conventional therapies often fail to meet clinical needs. Although non-coding RNAs are increasingly recognized as key regulators in cancer, the role of NKILA and its modulation by the miR-103/107 cluster in lung cancer growth and metastasis is not fully characterized. This study investigates the impact of the NKILA–miR-103/107 axis on lung cancer progression and metastatic behavior. Methods: To suppress miR-103 and miR-107 activity in the human lung cancer cell line A549, specific LNA-based inhibitors were introduced into the cells. Following in vitro transfection with either miR-specific LNA or a mock control, alterations in the components of the NKILA–miR-103/107 regulatory pathway were quantified using quantitative real-time PCR. The effects of miR inhibition on cellular behavior were then evaluated by measuring A549 cell growth with an MTT assay and assessing invasive capacity through a Transwell invasion test. Results: In lung cancer A549 cells, suppression of miR-103/107 using LNA inhibitors led to a marked elevation in NKILA transcript levels. Functional assays showed that miR-103/107 inhibition was associated with a significant decrease in A549 cell viability (p=0.0041) and a pronounced reduction in invasive capacity (p=0.001). Conclusion: In this in vitro study using A549 lung cancer cells, the NKILA–miR-103/107 axis was associated with lung cancer aggressiveness. miR-103/107 inhibition upregulated NKILA and was accompanied by decreased proliferation and invasion of A549 cells. These findings are preliminary and limited to a single cell line model. Further validation in additional lung cancer models and in vivo systems is required to determine the broader biological and therapeutic relevance of this regulatory interaction.

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