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Updated: Jul 3, 2025

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An Optimized Protocol for Electrophoretic Mobility Shift Assay Using Infrared Fluorescent Dye-labeled Oligonucleotides
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SOX2 Overlapping Transcript (SOX2-OT) Enhances the Lung Cancer Malignancy Through Interaction with miR-194-5p/SOX5
Zahra Sadeghi1, Fatemeh Dodangeh1, Jamshid Raheb1
1National Institute of Genetic Engineering and Biotechnology, Tehran, Iran.
Iranian Journal of Biotechnology
|February 12, 2024
Summary
This study reveals that the long non-coding RNA SOX2-OT promotes lung cancer malignancy by upregulating SOX5, beta-catenin, MMP9, and VEGF. Inhibiting SOX2-OT decreases these proteins, offering potential therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Lung cancer is a leading cause of cancer mortality globally.
- Identifying biomarkers for lung cancer malignancy is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of the long non-coding RNA SOX2-OT in regulating gene expression within lung cancer.
- To elucidate the molecular pathway involving SOX2-OT, miR-194-5p, and SOX5 in lung cancer progression.
Main Methods:
- A549 lung cancer cells were transfected with siRNA targeting SOX2-OT.
- Gene expression levels of SOX2-OT and miR-194-5p were quantified using real-time PCR.
- Protein expression levels of beta-catenin, MMP9, p-STAT3, SOX5, and VEGF were assessed via Western blotting.
Main Results:
- Silencing SOX2-OT led to increased miR-194-5p expression.
- A significant decrease in beta-catenin, SOX5, p-STAT3, VEGF, and MMP9 protein levels was observed post-SOX2-OT inhibition.
Conclusions:
- Elevated SOX2-OT expression in lung cancer correlates with increased levels of beta-catenin, SOX5, MMP9, and VEGF.
- These findings suggest that SOX2-OT promotes lung cancer malignancy by modulating this molecular pathway.
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