ArticleExperimental & molecular medicine2011
Up-regulation of BLT2 is critical for the survival of bladder cancer cells.
Article in Experimental & molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Immunoregulatory mechanisms of the arachidonic acid pathway in cancer.FEBS letters · 2025Review
- RNA methylation and cellular response to oxidative stress-promoting anticancer agents.Cell cycle (Georgetown, Tex.) · 2023Review
- Two distinct forms of human BLT2: long-form and short-form BLT2.Frontiers in cell and developmental biology · 2023Review
- Updates on the Pivotal Roles of Mitochondria in Urothelial Carcinoma.Biomedicines · 2022Review
- Magnesium isoglycyrrhizinate suppresses bladder cancer progression by modulating the miR-26b/Nox4 axis.Bioengineered · 2022Article
- A review of non-prostanoid, eicosanoid receptors: expression, characterization, regulation, and mechanism of action.Journal of cell communication and signaling · 2022Review
- A novel survival model based on a Ferroptosis-related gene signature for predicting overall survival in bladder cancer.BMC cancer · 2021Article
- Current updates on the role of reactive oxygen species in bladder cancer pathogenesis and therapeutics.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Review
- The yin and yang of leukotriene BSeminars in immunology · 2017Review
- Cross-Talk between Cancer Cells and the Tumour Microenvironment: The Role of the 5-Lipoxygenase Pathway.International journal of molecular sciences · 2017Review
- Review
- Leukotriene receptor expression in esophageal squamous cell cancer and non-transformed esophageal epithelium: a matched case control study.BMC gastroenterology · 2016Article
- LPS Up-Regulates ICAM-1 Expression in Breast Cancer Cells by Stimulating a MyD88-BLT2-ERK-Linked Cascade, Which Promotes Adhesion to Monocytes.Molecules and cells · 2015Article
- Article
- Ras promotes transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition via a leukotriene B4 receptor-2-linked cascade in mammary epithelial cells.The Journal of biological chemistry · 2014Article
- The role of chemoattractant receptors in shaping the tumor microenvironment.BioMed research international · 2014Review
- Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence.Immunology · 2013Article
- NADPH Oxidases NOXs and DUOXs as putative targets for cancer therapy.Anti-cancer agents in medicinal chemistry · 2013Review
- BLT2 is a pro-tumorigenic mediator during cancer progression and a therapeutic target for anti-cancer drug development.American journal of cancer research · 2013Article
- Aiding and abetting roles of NOX oxidases in cellular transformation.Nature reviews. Cancer · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence rates of urinary bladder cancer continue to rise yearly, and thus new therapeutic approaches and early diagnostic markers for bladder cancer are urgently needed. Thus, identifying the key mediators and molecular mechanisms responsible for the survival of bladder cancer has valuable implications for the development of therapy. In this study, the role of BLT2, a receptor for leukotriene B((4)) (LTB((4))) and 12(S)-hydroxyeicosatetraenoic acid (HETE), in the survival of bladder cancer 253J-BV cells was investigated. We found that the expression of BLT2 is highly elevated in bladder cancer cells. Also, we observed that blockade of BLT2 with an antagonist or BLT2 siRNA resulted in cell cycle arrest and apoptotic cell death, suggesting a role of BLT2 in the survival of human bladder cancer 253J-BV cells. Further experiments aimed at elucidating the mechanism by which BLT2 mediates survival revealed that enhanced level of reactive oxygen species (ROS) are generated via a BLT2-dependent up-regulation of NADPH oxidase members NOX1 and NOX4. Additionally, we observed that inhibition of ROS generation by either NOX1/4 siRNAs or treatment with an ROS-scavenging agent results in apoptotic cell death in 253J-BV bladder cancer cells. These results demonstrated that a 'BLT2-NOX1/4-ROS' cascade plays a role in the survival of this aggressive bladder cancer cells, thus pointing to BLT2 as a potential target for anti-bladder cancer therapy.
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