Avicenna journal of medical biotechnology · 2026
miR-103/107-Mediated Suppression of NKILA Enhances Oncogenic Behaviors in Human Lung Cancer Cells.
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Jafari Davood, Naghiloo Hossein, Athari Seyyed Shamsadin, Noorbakhsh Farshid, Rezaei Nima
Аннотация
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.
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.