DU145型
活力测定
细胞因子
自分泌信号
细胞培养
细胞
趋化因子
生物
白细胞介素8
癌症研究
癌细胞
化学
男科
细胞生物学
免疫学
癌症
医学
LNCaP公司
内科学
炎症
生物化学
遗传学
作者
Zarema Gilazieva,Gülçin Tezcan,Ekaterina Garanina,Nawar Sakr,Svetlana S. Arkhipova,L. S. Vinogradov,Albert A. Rizvanov,Svetlana F. Khaiboullina
出处
期刊:Blood
[Elsevier BV]
日期:2018-11-29
卷期号:132 (Supplement 1): 4964-4964
标识
DOI:10.1182/blood-2018-99-116076
摘要
Abstract Introduction: Interleukin 6 (IL-6) is proinflammatory cytokine which is produced by cell when Nod-like receptors (NLRs) are activated. Increased production of IL-6 was shown to promote tumor growth and metastasis.Therefore, it could be suggested that activation of NLRs could support malignancy. PC-3, prostate tumor derived cells, was shown to produce IL-6; however, little is known about the role of NLRs in regulation of cytokine secretion. Method: PC-3 cells were seeded in 48 well plate cell culture plates and culturd in presence of VX765, Nigericin or Camptothesin. After 24 hours incubation, cell death was determined using Annexin V test. Additionally, IL-6 level was assessed in culture medium using Bio-Plex Pro™ Human Chemokine Panel (Biorad). Data was analyzed using One Way Anova, Post Hoc Tukey test, SPSS 20. Results: Viability of PC3 cells was reduced when treated with Nigericin (37.74±0.33%) and Champtothesin (10.10±0.23%) as compared to untreated cells (P<0.01), while VX765 did not affect cell viability (4.78±0.28 %; P= 0.645). Nigerecin significatly increased IL-6 production in PC3 cells when compared to untreated cells. Interestingly, IL-6 levels in culture medium of PC3 cells treated with nigerecin was significantly higher than that in cells treated with VX765 and campthothesin (p< 0.001). Conclusion: It appears that IL-6 can be produced by PC3 cells upon stmulation of NLRs. Since NLRs activation was associated with reduced cell vitality, we suggest that increased IL-6 level in culture medium could be the result of the cytokine release from dead cells. This study was supported by RFBR Grant #18-34-01000 and Program of Competitive Growth of KFU. Disclosures No relevant conflicts of interest to declare.
科研通智能强力驱动
Strongly Powered by AbleSci AI