ArticleJournal of translational medicine2025
Smoking promotes the progression of bladder cancer through FOXM1/CKAP2L axis.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Pentachlorophenol enhances bladder cancer cell invasion through altered protein stability.iScience · 2026Article
- Smoking promotes colorectal cancer via the CKAP2L/AREG axis.International journal of oncology · 2026Article
- Predicting muscle-invasive bladder cancer with dual-layer detector spectral CT-derived extracellular volume fraction.BMC medical imaging · 2026Article
- Improvement of prognosis among patients with lung adenocarcinoma through precision therapy: analysis based on The Cancer Genome Atlas.Translational cancer research · 2026Article
- CKAP2L promotes endometrial cancer progression by suppressing AKT ubiquitination and activating the PI3K/AKT signaling pathway.Frontiers in oncology · 2026Article
- The Convergent Immunopathogenesis of Cigarette Smoke Exposure: From Oxidative Stress to Epigenetic Reprogramming in Chronic Disease.International journal of molecular sciences · 2025Review
- Observational
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundSmoking is a well-established risk factor for bladder cancer; however, the molecular mechanisms underlying this association remain unclear. This study aimed to elucidate the link between smoking and bladder cancer and identify the molecular mechanisms by which smoking promotes tumor progression.
methodsThe relationships between smoking and bladder cancer were assessed with cross-sectional analyses and Mendelian randomization (MR) analyses. Bioinformatics analyses were conducted to identify the key genes involved in smoking-induced bladder cancer progression. Following treatment of bladder cancer cells with cigarette smoke extract (CSE), the effects of CKAP2L on proliferation and metastasis were evaluated using in vitro proliferation, migration, and invasion assays, as well as an in vivo subcutaneous tumor model. FOXM1 binding to the CKAP2L promoter was determined by chromatin immunoprecipitation (ChIP) assay.
resultsBoth cross-sectional and MR analyses confirmed the positive relationship between smoking and bladder cancer. Functional experiments revealed that CSE treatment promoted the proliferation and metastasis of bladder cancer cells. CKAP2L was identified as a key gene by bioinformatics analyses, and its expression was upregulated by CSE treatment. Additionally, CKAP2L knockdown inhibited cell proliferation, migration, and invasion; arrested the cell cycle at the S and G2/M phases; and regulated the expression of related proteins. Overexpression of CKAP2L exhibited the opposite results. The ChIP‒qPCR assay confirmed significant binding of FOXM1 to the CKAP2L promoter.
conclusionSmoking promoted bladder cancer progression by upregulating CKAP2L and FOXM1, which drive tumor progression via cell cycle regulation. This identifies the FOXM1/CKAP2L axis as a mechanism by which smoking facilitates bladder cancer progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.