ArticleCancer cell international2023
SQLE Knockdown inhibits bladder cancer progression by regulating the PTEN/AKT/GSK3β signaling pathway through P53.
Article in Cancer cell international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Therapeutic potential of asparagus polysaccharide in bladder cancer treatment via modulation of PI3K/AKT/mTOR signaling.Scientific reports · 2026Article
- SQLE drives bladder cancer progression by boosting mitochondrial oxidative phosphorylation.Oncogene · 2025Article
- Decoding the cholesterol-apoptosis axis in HCC: a machine learning-based multi-omics integration and single-cell transcriptomic analysis.Discover oncology · 2025Article
- A novel, synthesized, amphiphilic ethylene glycol squalene derivative suppresses BBN-induced bladder carcinogenesis.Scientific reports · 2025Article
- Hypoxia-induced HIF-1α/VASN promotes bladder cancer progression.Scientific reports · 2025Article
- Review of recent molecular pathology of bladder urothelial carcinoma.Discover oncology · 2025Review
- Inhibition of KDM4A restricts SQLE transcription and induces oxidative stress imbalance to suppress bladder cancer.Redox biology · 2024Article
- Squalene monooxygenase (SQLE) protects ovarian cancer cells from ferroptosis.Scientific reports · 2024Article
- Review
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Bladder cancer (BCa) is one of the most common malignancies worldwide. However, the lack of accurate and effective targeted drugs has become a major problem in current clinical treatment of BCa. Studies have demonstrated that squalene epoxidase (SQLE), as a key rate-limiting enzyme in cholesterol biosynthesis, is involved in cancer development. In this study, our analysis of The Cancer Genome Atlas, The Genotype-Tissue Expression, and Gene Expression Omnibus databases showed that SQLE expression was significantly higher in cancer tissues than it was in adjacent normal tissues, and BCa tissues with a high SQLE expression displayed a poor prognosis. We then confirmed this result in qRT-PCR and immunohistochemical staining experiments, and our vitro studies demonstrated that SQLE knockdown inhibited tumor cell proliferation and metastasis through the PTEN/AKT/GSK3β signaling pathway. By means of rescue experiments, we proved that that P53 is a key molecule in SQLE-mediated regulation of the PTEN/AKT/GSK3β signaling pathway. Simultaneously, we verified the above findings through a tumorigenesis experiment in nude mice. In conclusion, our study shows that SQLE promotes BCa growth through the P53/PTEN/AKT/GSK3β axis, which may serve as a therapeutic biological target for BCa.
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