1. Aspirin exerts anti-tumor effect through inhibiting Blimp1 and activating ATF4/CHOP pathway in multiple myeloma
- Author
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Ting Sun, Chao Xiong, Jie Geng, Yuqing Li, Jun-Wen Liu, Xuebing Li, Hongchun Liu, and Zhenzhen Ren
- Subjects
0301 basic medicine ,Blimp1 ,Antineoplastic Agents ,Apoptosis ,RM1-950 ,CHOP ,Mitochondrion ,03 medical and health sciences ,0302 clinical medicine ,Multiple myeloma ,Cell Line, Tumor ,Humans ,ATF4 ,Receptor ,Cell Proliferation ,Pharmacology ,Dose-Response Relationship, Drug ,Aspirin ,Chemistry ,Endoplasmic reticulum ,General Medicine ,Activating Transcription Factor 4 ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,030220 oncology & carcinogenesis ,Gene Knockdown Techniques ,Cancer research ,Unfolded protein response ,Positive Regulatory Domain I-Binding Factor 1 ,Therapeutics. Pharmacology ,Signal transduction ,Transcription Factor CHOP ,Signal Transduction - Abstract
B lymphocyte-induced maturation protein-1 (Blimp1) is a key regulator that promotes the terminal differentiation of mature B lymphocytes into plasma cells, and is essential for the survival of Multiple myeloma (MM)cells. However, the expression of Blimp1 in MM and its effect on the signaling pathway remain unknown. Studies have found that during long-term endoplasmic reticulum (ER) stress, activated ATF4 may also stimulate the CCAAT-enhancer-binding protein homologous protein (CHOP) gene, triggering the unfolded protein response (UPR) terminal apoptotic pathway in plasma cells. Moreover Aspirin can induce MM cell apoptosis through mitochondria and death receptor pathway. Therefore, we aim to explore whether Aspirin could induce AFT4/CHOP apoptosis pathway in MM by inhibiting Blimp1 expression, thereby promoting MM cell apoptosis and exerting anti-tumor effects.
- Published
- 2020