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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Antineoplastic Agents, Apoptosis, Caspases, Cell Line, Tumor, Cell Proliferation, Dose-Response Relationship, Drug, Enzyme Activation, Humans, JNK Mitogen-Activated Protein Kinases, Lymphoma, Primary Effusion, Reactive Oxygen Species, Sodium Salicylate, p38 Mitogen-Activated Protein Kinases.
user
Does potent reactive oxygen species-JNK-p38 activation by sodium salicylate potentiate death of primary effusion lymphoma cells? Context: Primary effusion lymphoma (PEL) is a rare but aggressive form of non-Hodgkin's B-cell lymphoma in immunodeficient patients. Resistance to conventional chemotherapeutic regimens is common in PEL and contributes to a very poor prognosis; hence, novel potent anti-PEL agents are required. Anticancer effects of non-steroidal anti-inflammatory drugs (NSAIDs) are well-established in epithelial cancer but are unclear in hematological malignancies. Therefore, the anticancer activities of selected NSAIDs, sodium salicylate (NaS), on PEL cell lines are of interest. Anti-proliferation of NaS on PEL cell lines was shown by MTT. Apoptosis induction and caspase activations were determined by flow cytometry analysis. ROS production was accessed by DCFH-DA. Western blot was performed to determine molecular mechanisms. NaS effectively inhibited cell proliferation of all PEL cell lines. Caspase-dependent apoptosis was demonstrated and simultaneous induction of reactive oxygen species production and c-Jun N-terminal kinases (JNK)-p38 activation was observed prior to apoptosis induction, and these might be responsible for NaS-induced apoptosis.
assistant
Significant anticancer effects of NaS on PEL cell lines were found. A novel role of NaS for PEL treatment is suggested. Final Decision: yes