ArticleScientific reports2024
BUB1 induces AKT/mTOR pathway activity to promote EMT induction in human small cell lung cancer.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- BUB1 regulates cell proliferation and apoptosis in cervical cancer by AKT signaling and autophagosome-lysosome fusion via ACTN1.iScience · 2026Article
- BUB1 in cancer genetics and oncogenomics: from chromosomal instability to therapeutic vulnerabilities.Frontiers in genetics · 2026Review
- BUB1 an Overexpressed Kinase in Sarcoma: Finding New Target Therapy for Osteosarcoma, Liposarcoma, Synovial Sarcoma, and Leiomyosarcoma.Biomolecules · 2025Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small cell lung cancer (SCLC) is a very aggressive tumor. Abnormal expression of BUB1 has been reported in several cancer types, wherein it plays a range of functional roles. This work aimed to elucidate the functional significance and molecular impacts of BUB1 in SCLC. It was found that SCLC cell lines exhibited significant BUB1 upregulation relative to control bronchial cells using data from the Gene Expression Omnibus (GEO) database and verified by immunohistochemical staining. BUB1 was also found to promote the proliferative, migratory, invasive activity of SCLC cells, as shown by CCK-8, 3D migration wound-healing, and Transwell assays, as well as flow cytometry. Additionally, it was found that BUB1 silencing enhanced E-cadherin expression while suppressing N-cadherin, Vimentin, ZEB-1, and Snail levels, as shown by Western immunoblotting. The loss of BUB1 also reduced p-AKT and p-mTOR levels without altering total AKT or mTOR protein levels. In conclusion, BUB1 functions as an oncogenic promoter in SCLC, potentially regulating the epithelial-mesenchymal transition by activation of AKT/mTOR signaling.
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