Abstract 6684: Aiolos expression regulates epithelial-mesenchymal transition through repressing miR-424-5p in lung cancer cells

Abstract Introduction: Epithelial-mesenchymal transition (EMT) is one of the major molecular mechanisms inducing tumor invasion and metastasis. The Ikaros family of DNA binding proteins are zinc finger transcription factors. Aiolos overexpression promotes EMT through upregulating the PI 3-kinase/Akt/Twist/MMP16 pathway in lung cancer. However, the roles of Aiolos regulating EMT and metastasis through miRNAs expression in lung cancer has not been well demonstrated in the literature. Materials and Methods: qRT-PCR was performed to determine miR-424-5p expression in H1299-Aiolos and A549-Aiolos cells. Knockdown of miR-424-5p was performed in H1299 cells, and transfection of miR-424-5p was performed in A549 cells. Western blotting analysis was performed to demonstrated E-cadherin and vimentin expression. Migration assay and matrigel invasion assay were done to determine the EMT phenotypes after miR-424-5p transfection or knockdown in lung cancer cells. Results: Down-regulation of miR-424-5p in H1299-Aiolos and A549-Aiolos cells was determined by qRT-PCR. Western blotting analysis showed decreased E-cadherin and increased vimentin expression in H1299 cells after miR-424-5p knockdown. Western blotting analysis also showed increased E-cadherin and decreased vimentin expression in A549 cells after miR-424-5p transfection. Migration assay showed that migration increased in H1299-shmiR-424-5p cells, but decreased in A549-miR-424-5p cells. Matrigel invasion assay showed the invasiveness increased in H1299-shmiR-424-5p cells, but decreased in A549-miR-424-5p cells. Conclusions: Aiolos expression regulates EMT through repressing miR-424-5p expression in lung cancer cells. The results shed light on further understanding of the mechanisms of metastasis in lung cancer. Citation Format: Ying-Shiun Kao, Jung-Jyh Hung. Aiolos expression regulates epithelial-mesenchymal transition through repressing miR-424-5p in lung cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 6684.

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Journal
Cancer Research
Published
2025-04-21
DOI
https://doi.org/10.1158/1538-7445.am2025-6684
Primary Topic
Cancer-related molecular mechanisms research
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article
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article

Abstract 6684: Aiolos expression regulates epithelial-mesenchymal transition through repressing miR-424-5p in lung cancer cells

Ying-Shiun Kao, Jung‐Jyh Hung
Cancer Research
Cancer-related molecular mechanisms research
article

Abstract 6684: Aiolos expression regulates epithelial-mesenchymal transition through repressing miR-424-5p in lung cancer cells

Ying-Shiun Kao, Jung‐Jyh Hung
article en

Abstract

Abstract Introduction: Epithelial-mesenchymal transition (EMT) is one of the major molecular mechanisms inducing tumor invasion and metastasis. The Ikaros family of DNA binding proteins are zinc finger transcription factors. Aiolos overexpression promotes EMT through upregulating the PI 3-kinase/Akt/Twist/MMP16 pathway in lung cancer. However, the roles of Aiolos regulating EMT and metastasis through miRNAs expression in lung cancer has not been well demonstrated in the literature. Materials and Methods: qRT-PCR was performed to determine miR-424-5p expression in H1299-Aiolos and A549-Aiolos cells. Knockdown of miR-424-5p was performed in H1299 cells, and transfection of miR-424-5p was performed in A549 cells. Western blotting analysis was performed to demonstrated E-cadherin and vimentin expression. Migration assay and matrigel invasion assay were done to determine the EMT phenotypes after miR-424-5p transfection or knockdown in lung cancer cells. Results: Down-regulation of miR-424-5p in H1299-Aiolos and A549-Aiolos cells was determined by qRT-PCR. Western blotting analysis showed decreased E-cadherin and increased vimentin expression in H1299 cells after miR-424-5p knockdown. Western blotting analysis also showed increased E-cadherin and decreased vimentin expression in A549 cells after miR-424-5p transfection. Migration assay showed that migration increased in H1299-shmiR-424-5p cells, but decreased in A549-miR-424-5p cells. Matrigel invasion assay showed the invasiveness increased in H1299-shmiR-424-5p cells, but decreased in A549-miR-424-5p cells. Conclusions: Aiolos expression regulates EMT through repressing miR-424-5p expression in lung cancer cells. The results shed light on further understanding of the mechanisms of metastasis in lung cancer. Citation Format: Ying-Shiun Kao, Jung-Jyh Hung. Aiolos expression regulates epithelial-mesenchymal transition through repressing miR-424-5p in lung cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 6684.

Cancer ResearchVol. 85(8_Supplement_1)
Taipei Veterans General Hospital (TW)
Openalex Percentile: Top 90%
Cancer-related molecular mechanisms research
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