ArticleOncology letters2014
Tumor necrosis factor-α-induced a disintegrin and metalloprotease 10 increases apoptosis resistance in prostate cancer cells.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- "Cytokine-Mediated tumor sensitization: mechanistic frameworks and therapeutic opportunities in cancer Immunotherapy".Clinical and experimental medicine · 2026Review
- ADAM10-cleaved ephrin-A5 contributes to prostate cancer metastasis.Cell death & disease · 2022Article
- The involvement of FBP1 in prostate cancer cell epithelial mesenchymal transition, invasion and metastasis by regulating the MAPK signaling pathway.Cell cycle (Georgetown, Tex.) · 2019Article
- An ADAM10 promoter polymorphism is a functional variant in severe sepsis patients and confers susceptibility to the development of sepsis.Critical care (London, England) · 2015Article
- Changes of HMGB1 and sRAGE during the recovery of COPD exacerbation.Journal of thoracic disease · 2014Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In developed countries, prostate cancer (PCa) is the second most frequently diagnosed type of cancer and the third most common cause of cancer-related mortality in males. Compared with western countries, the morbidity rate of PCa in China is markedly lower, however, it is rising annually. The etiology of PCa is unclear, therefore, to investigate how a disintegrin and metalloprotease 10 (ADAM10) functions in PCa, ADAM10 mRNA and protein levels induced by tumor necrosis factor (TNF)-α were identified using polymerase chain reaction and flow cytometry, respectively. To investigate the mechanism of ADAM10 activity in PCa, specific inhibitors were used, and DNA transfection and RNA interference technology were employed to identify the interaction between ADAM10 and the Fas ligand (L). The results indicated that TNF-α induced ADAM10 expression in a time- and dose-dependent manner through the p38 mitogen-activated protein kinase/necrosis factor-κB signaling pathway. ADAM10 hydrolyzed FasL and contributed to apoptosis resistance of the tumor cells. These observations indicate a promising therapeutic modality for the treatment of apoptosis-resistant PCa, by targeting ADAM10 sheddase activity.
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Registered trials
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