ArticleOncology letters2017
Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Cigarette smoking and risk of bladder cancer: a dose-response meta-analysis.International urology and nephrology · 2022Pooled it
- Exosomal circ55033 promotes cigarette smoke-induced bladder cancer by modulating EMT and stem cell properties.Medical oncology (Northwood, London, England) · 2026Article
- Effects of Nicotine on Urinary Bladder Carcinogenesis.Pathology international · 2026Review
- Assessing the Impact ofWorld journal of oncology · 2025Article
- Twenty-five years of WWOX insight in cancer: a treasure trove of knowledge.Functional & integrative genomics · 2025Review
- The role of smoking in bladder cancer risk: Unveiling racial and ethnic disparities in US and global populations, a secondary dataset analysis.Tobacco induced diseases · 2025Article
- Hesperidin inhibits tobacco smoke-induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway.Oncology letters · 2023Article
- DNA Damage and Oxidative Stress of Tobacco Smoke Condensate in Human Bladder Epithelial Cells.Chemical research in toxicology · 2022Article
- Diallyl trisulfide inhibited tobacco smoke-mediated bladder EMT and cancer stem cell marker expression via the NF-κB pathwayThe Journal of international medical research · 2021Article
- High-Risk Human Papillomavirus and Tobacco Smoke Interactions in Epithelial Carcinogenesis.Cancers · 2020Review
- Cigarette smoke downregulates Nur77 to exacerbate inflammation in chronic obstructive pulmonary disease (COPD).PloS one · 2020Article
- Resveratrol Reverses Cigarette Smoke-Induced Urocystic Epithelial-Mesenchymal Transition via Suppression of STAT3 Phosphorylation in SV-HUC-1-Immortalized Human Urothelial Cells.OncoTargets and therapy · 2019Article
- Duration-dependent effects of nicotine exposure on growth and AKT activation in human kidney epithelial cells.Molecular and cellular biochemistry · 2018Article
- Tobacco Exposure Enhances Human Papillomavirus 16 Oncogene Expression via EGFR/PI3K/Akt/c-Jun Signaling Pathway in Cervical Cancer Cells.Frontiers in microbiology · 2018Article
- Secondhand smoking increases bladder cancer risk in nonsmoking population: a meta-analysis.Cancer management and research · 2018Review
- Role of AP-1 in the tobacco smoke-induced urocystic abnormal cell differentiation and epithelial-mesenchymal transitionInternational journal of clinical and experimental pathology · 2017Article
- Recuperating Lung Decoction Attenuates the Oxidative Stress State of Chronic Obstructive Pulmonary Disease by Inhibiting the MAPK/AP-1 Signal Pathway and RegulatingEvidence-based complementary and alternative medicine : eCAM · 2017Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer (BC) is universally acknowledged as a significant public health issue, worldwide. Numerous studies have demonstrated that cigarette smoke is the primary risk factor for BC. However, the mechanism of cigarette smoke-induced BC has not been fully elucidated. Sustained epithelial cell hyperplasia has been identified as a preneoplastic lesion during the formation of BC. The aim of the present study was to investigate whether exposure to cigarette smoke extract (CSE) induced proliferation in normal human urothelial SV-HUC-1 cells. Furthermore, the role of the mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) pathway in the CSE-induced proliferation of SV-HUC-1 cells was also investigated. The present study revealed that the expression of phosphorylated-extracellular signal regulated protein kinase (ERK)1/2, Jun N-terminal kinase (JNK) and p38 was significantly increased following exposure to CSE in SV-HUC-1 cells. Furthermore, CSE increased the expression of the proliferation markers, cyclin D1 and proliferating cell nuclear antigen. By contrast, CSE attenuated the expression of p21. In addition, the inhibitors of ERK1/2 and JNK reversed the aforementioned effects of CSE. However, p38 inhibition did not reverse CSE-induced proliferation. In conclusion, the results of the present study demonstrated that exposure to CSE induced proliferation in normal human urothelial cells. Furthermore, the results also indicated that the ERK1/2 and JNK pathways are important for the regulation of proliferation via the AP-1 proteins.
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