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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: OBJECTIVE, METHODS, RESULTS. Meshes: Apoptosis, DNA-Binding Proteins, Humans, Interleukin-6, Janus Kinase 2, Mitogen-Activated Protein Kinases, Multiple Myeloma, Myeloid Cell Leukemia Sequence 1 Protein, Neoplasm Proteins, Phosphatidylinositol 3-Kinases, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, STAT1 Transcription Factor, STAT3 Transcription Factor, Signal Transduction, Trans-Activators, Tumor Cells, Cultured, Up-Regulation.
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Does iL-6 inhibit apoptosis of human myeloma cell line XG-7 through activation of JAK/STAT pathway and up-regulation of Mcl-1? Context: IL-6 can protect myeloma cells from apoptosis induced by various stimuli. A series of intracellular molecules might participate in this process. Our aim in this study is to investigate which anti-apoptotic Bcl-2 family proteins (Bcl-2, Bcl-XL, Mcl-1) and which signal transduction pathway(JAK/STAT, Ras/MAPK, PI-3K/Akt) can mediate the anti-apoptotic effect of IL-6 on a human myeloma cell line XG-7. Apoptosis of XG-7 cells was analyzed by flow cytometry with propidium iodide(PI) staining of nuclei. The expression of three Bcl-2 family proteins in XG-7 cells were monitored by immunoblot assay. AG490, PD98059, and LY294002, three specific antagonists for JAK/STAT, Ras/MAPK, and PI-3K/Akt signal transduction pathways respectively, were used to determine which signal transduction pathway was responsible for the effect of IL-6 on XG-7 cells. IL-6 inhibited the apoptosis of XG-7 cells and up-regulated the expression of only one of the three anti-apoptotic Bcl-2 family proteins-Mcl-1. In addition, up-regulation of Mcl-1 expression induced by IL-6 was significantly inhibited in the presence of AG490, while not of PD98059 and LY294002.
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IL-6 inhibited apoptosis of XG-7 cells through up-regulation of Mcl-1 and the activation of JAK/STAT rather than Ras/MAPK nor PI-3K/Akt signal transduction pathway. Final Decision: yes