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首页> 外文期刊>Cell Research >Bcl-2 down modulation in WEHI-3B/CTRES cells resistant to Cholera Toxin (CT)-induced apoptosis.
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Bcl-2 down modulation in WEHI-3B/CTRES cells resistant to Cholera Toxin (CT)-induced apoptosis.

机译：Bcl-2下调对霍乱毒素（CT）诱导的细胞凋亡的WEHI-3B / CTRES细胞。

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The very different effects of Cholera Toxin (CT) on cell growth and proliferation may depend on the type of ganglioside receptors in cell membranes and different signal transduction mechanisms triggered, but other functions related to the drug resistance mechanisms can not be excluded. The effect of CT treatment on the "in vitro" clonogenicity, the Population Doubling Time (PDT), apoptosis, PKA activation and Bax and Bcl-2 expression was evaluated in WEHI-3B cell line and its CT-resistant subclone (WEHI-3B/CTRES). In WEHI-3B parental cells the dramatic accumulation of cAMP induced by CT correlated well with PKA activation, increased PDT value, inhibition of clonogenicity and apoptosis. H-89 treatment inhibited PKA activation by CT but did not protect the cells from apoptosis and growth inhibition. In WEHI-3B/CTRES no significant CT-dependent accumulation of cAMP occurred with any increase of PKA activity and PDT. In CT resistant cells (WEHI-3B/CTRES), Bcl-2 expression was down regulated by both CT or drug treatment (eg., ciprofloxacin, CPX) although these cells were protected from CT-dependent apoptosis but not from drug-induced apoptosis. Differently from other cell models described, down regulation of Bcl-2 is proved to be independent on cAMP accumulation and PKA activation. Our observations support the implication of cAMP dependent kinase (PKA) in the inhibition of WEHI-3B cells growth and suggest that, in WEHI-3B/CTRES, Bcl-2 expression could be modulated by CT in the absence of cAMP accumulation. Also in consideration of many contradictory data reported in literature, our cell models (of one sensitive parental cell strain and two clones with different uncrossed specific resistance to CT and CPX) provides a new and interesting tool for better investigating the relationship between the CT signal transduction mechanisms and Bcl-2 expression and function.Cell Research (2006) 16: 306-312. doi:10.1038/sj.cr.7310038; published online 16 March 2006.
机译：霍乱毒素（CT）对细胞生长和增殖的不同影响可能取决于细胞膜中神经节苷脂受体的类型和触发的不同信号转导机制，但不能排除与耐药机制有关的其他功能。在WEHI-3B细胞系及其耐CT耐药的亚克隆（WEHI-3B）中评估了CT处理对“体外”克隆形成性，群体倍增时间（PDT），凋亡，PKA活化以及Bax和Bcl-2表达的影响。 / CTRES）。在WEHI-3B亲本细胞中，CT诱导的cAMP的大量积累与PKA激活，PDT值增加，克隆形成性和凋亡抑制密切相关。 H-89处理可抑制CT激活PKA，但不能保护细胞免于凋亡和生长抑制。在WEHI-3B / CTRES中，随着PKA活性和PDT的增加，没有明显的CT依赖的cAMP积累发生。在CT耐药细胞（WEHI-3B / CTRES）中，Bcl-2的表达受CT或药物治疗（例如环丙沙星，CPX）均下调，尽管这些细胞不受CT依赖性细胞凋亡的保护，但不受药物诱导的细胞凋亡的保护。与描述的其他细胞模型不同，已证明Bcl-2的下调独立于cAMP积累和PKA激活。我们的观察结果支持cAMP依赖性激酶（PKA）抑制WEHI-3B细胞的生长，并暗示在WEHI-3B / CTRES中，在不存在cAMP积累的情况下，CT可以调节Bcl-2的表达。同样考虑到文献中报道的许多矛盾数据，我们的细胞模型（一个敏感的亲代细胞株和两个对CT和CPX具有不同的未交叉特异性抗性的克隆）提供了一个新的有趣的工具，可以更好地研究CT信号转导之间的关系机理以及Bcl-2表达和功能.Cell Research（2006）16：306-312。 doi：10.1038 / sj.cr.7310038;在线发布于2006年3月16日。

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