ArticleJournal of cancer research and clinical oncology2019
Possible correlation of sonic hedgehog signaling with epithelial-mesenchymal transition in muscle-invasive bladder cancer progression.
Article in Journal of cancer research and clinical oncology, 2019. 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.
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Immunohistochemical study of Rho-kinase pathway expression in a mouse model of prostate hypertrophy for preliminary study of progressive prostate cancer model establishment.Translational andrology and urology · 2025Article
- Primary cilia and cancer: a tale of many faces.Oncogene · 2025Review
- Article
- Combined Treatment with Ultrasound and Immune Checkpoint Inhibitors for Prostate Cancer.Journal of clinical medicine · 2022Article
- Sonic Hedgehog signaling pathway in gynecological and genitourinary cancer (Review).International journal of molecular medicine · 2021Review
- Primary cilia presence and implications in bladder cancer progression and invasiveness.Histochemistry and cell biology · 2021Article
- Nanaomycin K inhibited epithelial mesenchymal transition and tumor growth in bladder cancer cells in vitro and in vivo.Scientific reports · 2021Article
- Understanding the Hedgehog Signaling Pathway in Acute Myeloid Leukemia Stem Cells: A Necessary Step toward a Cure.Biology · 2021Review
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
purposeTo investigate the role of sonic hedgehog (Shh) signaling and epithelial-mesenchymal transition (EMT) in bladder cancer progression and invasion.
methodsWe cultured three bladder cancer cell lines, muscle-invasive T24 and 5637, and non-muscle-invasive KK47, in the presence of a recombinant-Shh (r-Shh) protein or cyclopamine, a Shh signaling inhibitor, to investigate proliferation and expression of EMT markers. Wound-healing assays and transwell assay were performed to evaluate cell invasion and migration. Mice were then inoculated with bladder cancer cells and treated with cyclopamine. Mouse tumor samples were stained for Shh signaling and EMT markers.
resultsR-Shh protein enhanced cell proliferation, whereas cyclopamine significantly suppressed cell proliferation, especially in invasive cancer (5637 and T24) (p < 0.05). R-Shh protein promoted EMT, suppressed E-cadherin and enhanced N-cadherin and vimentin and Gli1, an Shh downstream molecule, while cyclopamine blocked EMT, especially in 5637 and T24. Cyclopamine also inhibited cell invasion and migration in vitro. In the animal study, intraperitoneal injection of cyclopamine significantly suppressed tumor growth in 5637 and T24 in mice (p = 0.01 and p = 0.004, respectively) and slightly suppressing KK47 tumor growth (p = 0.298). Significant cyclopamine-induced suppression of Gli1 in 5637 and T24 mouse tumors (both p = 0.03) was seen, suggesting that muscle-invasive bladder cancer may be more dependent on Shh signaling than non-muscle-invasive bladder cancer.
conclusionsShh signaling and EMT were especially enhanced in muscle-invasive bladder cancer progression and invasion, and suppressed by the inhibition of Shh signaling.
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