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Updated: Aug 5, 2026
Direct Measurement of KDM1A Target Engagement Using Chemoprobe-based Immunoassays
Published on: June 13, 2019
Integrated Bioinformatic and Experimental Analysis Reveals the Molecular Mechanisms Underlying KDM1B/LSD2 Inhibition
Kayalvizhi Samuvel Muthiah1, Sathan Raj Natarajan2, Udesh Dhawan3
1Department of Chemical Engineering and Biotechnology, National Taipei University of Technology (Taipei Tech), Taipei, Taiwan.
Abstract:
Lung cancer remains a major global health challenge, and the oncogenic function of KDM1B (Lysine-specific Demethylase 1B) is still poorly characterized. This study employed integrated bioinformatics and experimental approaches to investigate KDM1B's function in lung cancer. Pan-cancer analysis using databases such as TIMER revealed notably elevated KDM1B mRNA expression in LUAD datasets, suggesting its potential as a diagnostic biomarker. A strong association was also found between increased KDM1B levels and immune cell infiltration in LUAD datasets. Protein interaction networks constructed using STRING and Cytoscape revealed close associations between KDM1B and key regulatory genes in NSCLC. KEGG enrichment analysis linked KDM1B to the mTOR signaling, which is critical for cell proliferation and survival. RT-PCR and western blotting for experimental validation showed KDM1B expression was significantly increased in A549 and NCI-H460 lung cancer cells. The deletion of KDM1B inhibits cell growth, induces G0/G1 phase cell cycle arrest, and promotes apoptosis in A54 cells. Moreover, cell proliferation was significantly inhibited by the KDM1B inhibitor, tranylcypromine, and induced G0/G1 phase cell cycle arrest, increased apoptosis, ROS, and glycolytic activity in A549 cells. Collectively, these findings highlight KDM1B as a valuable therapeutic target in lung adenocarcinoma and emphasize its key role in lung cancer development.
Insights
Lysine-specific demethylase 1B (KDM1B) is elevated in lung adenocarcinoma, promoting cancer growth and survival. Inhibiting KDM1B halts proliferation and induces cell death, marking it as a promising therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- Lung cancer is a significant global health issue.
- The role of Lysine-specific demethylase 1B (KDM1B) in lung cancer oncogenesis is not well understood.
- Identifying novel therapeutic targets is crucial for improving lung cancer treatment outcomes.
Purpose of the Study:
- To investigate the function and therapeutic potential of KDM1B in lung cancer.
- To explore KDM1B's association with diagnostic biomarkers and immune cell infiltration in lung adenocarcinoma (LUAD).
- To validate KDM1B's role in lung cancer cell proliferation, cell cycle, and apoptosis.
Main Methods:
- Integrated bioinformatics analysis of pan-cancer datasets (TIMER, STRING, Cytoscape, KEGG).
- Experimental validation using RT-PCR and Western blotting in lung cancer cell lines (A549, NCI-H460).
- Functional assays including gene deletion, cell cycle analysis, apoptosis assays, and treatment with a KDM1B inhibitor (tranylcypromine).
Main Results:
- KDM1B mRNA expression is significantly elevated in LUAD datasets and associated with immune cell infiltration.
- KDM1B interacts with key regulatory genes in non-small cell lung cancer (NSCLC) and is linked to mTOR signaling.
- KDM1B deletion or inhibition in lung cancer cells suppressed proliferation, induced G0/G1 cell cycle arrest, promoted apoptosis, and increased ROS and glycolytic activity.
Conclusions:
- KDM1B plays a critical oncogenic role in lung adenocarcinoma development.
- KDM1B is a potential diagnostic biomarker and a promising therapeutic target for lung cancer.
- Targeting KDM1B offers a viable strategy for inhibiting lung cancer cell growth and inducing cell death.
