ArticleCancer gene therapy2022
LSD1-mediated stabilization of SEPT6 protein activates the TGF-β1 pathway and regulates non-small-cell lung cancer metastasis.
Article in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 47 citations in OpenAlex.
- Epigenetics in lung cancer precision medicine: from bench to bedside-a narrative review.Translational lung cancer research · 2026Review
- Article
- Role of lysine-specific demethylase 1 in immunotherapy of gastric cancer: An update.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024Article
- Targeting Group 3 Medulloblastoma by the Anti-PRUNE-1 and Anti-LSD1/KDM1A Epigenetic Molecules.International journal of molecular sciences · 2024Article
- Review
- LSD1: an emerging face in altering the tumor microenvironment and enhancing immune checkpoint therapy.Journal of biomedical science · 2023Review
- Article
- Article
- Review
- Relationship between histone demethylase LSD family and development and prognosis of gastric cancer.Frontiers in immunology · 2023Review
- The role of miR-145-5p in esophageal squamous cell carcinoma tumor-associated macrophages and selection of immunochemotherapy.Journal of thoracic disease · 2022Article
- Epigenetic modification regulates tumor progression and metastasis through EMT (Review).International journal of oncology · 2022Review
- Sanguinarine, identified as a natural alkaloid LSD1 inhibitor, suppresses lung cancer cell growth and migration.Iranian journal of basic medical sciences · 2022Article
- UBC Mediated by SEPT6 Inhibited the Progression of Prostate Cancer.Mediators of inflammation · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is a prevalent cancer with unfavorable prognosis. Over the past decade accumulating studies have reported an involvement of lysine-specific histone demethylase 1 (LSD1) in NSCLC development. Here, we aimed to explore whether LSD1 affects the metastasis of NSCLC by mediating Septin 6 (SEPT6) through the TGF-β1 pathway. RT-qPCR was used to determine LSD1 and SEPT6 expression in NSCLC tissues and cells. Interactions between LSD1, SEPT6, and TGF-β1 were detected using lentivirus-mediated silencing of LSD1 and overexpression of SEPT6. The role of LSD1 and SEPT6 in mediating the biological behavior of NSCLC cells was determined using the EdU proliferation assay, Transwell assay, and flow cytometry. Thereafter, transplanted cell tumors into nude mice were used to explore the in vivo effects of LSD1 and SEPT6 on metastasis of NSCLC. LSD1 and SEPT6 were overexpressed in NSCLC tissue and cell samples. LSD1 could demethylate the promoter of the SEPT6 to positively regulate SEPT6 expression. LSD1 promoted proliferation, migration, and invasion, while suppressing the apoptosis of NSCLC cells by increasing SEPT6 expression. LSD1-mediated SEPT6 accelerated in vivo NSCLC metastasis through the TGF-β1/Smad pathway. Collectively, LSD1 demethylates SEPT6 promoter to upregulate SEPT6, which activates TGF-β1 pathway, thereby promoting metastasis of NSCLC.
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