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首页> 外文期刊>Journal of Cellular Physiology >Celastrol and Attenuation of Tumor Growth in Systemic Malignancies: A Clinical Perspective
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Celastrol and Attenuation of Tumor Growth in Systemic Malignancies: A Clinical Perspective

机译：Celastrol和衰减的肿瘤生长全身恶性肿瘤:临床的视角

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Wang et al. [2012] have provided interesting data in their recent article. Interestingly, celastrol exerts significant anti-neoplastic effects in other systemic malignancies.For instance, celastrol inhibits tumor growth in breast malignancies. It acts by attenuating NF-KB-mediated MMP-9 expression in the cancerous cells (Kim et al., 2011). This markedly attenuates tumor invasiveness as well as metastasis. kBa degradation is also decreased resulting in further decrease in tumor growth. Proliferation is thus inhibited by modulation of a mitochondrial dependent caspase pathway. Bax levels are typically up-regulated (Yang et al., 201 I). On the other hand, Bcl-2 levels are down- regulated. Increased PARP cleavage accompanies these changes and further augments tumor growth inhibition. Besides these effects, celastrol also modulates the estrogen receptor a thus further inhibiting tumor growth. It attenuates estrogen receptor a transcription Gang et al., 2011).Similar effects have been seen in non-small cell lung carcinomas. It mediates this effect by activation of FasL mediated apoptosis. At the same time, it also induces mitochondrial mediated apoptosis in the cancerous cells. Mitochondrial membrane potential is attenuated markedly. Simultaneously, it decreases Bcl-2 expression while increasing Bax expression within the tumor cells (Mou et al., 201 I). Caspase-3 cleavage is also augmented resulting in further enhancement of apoptosis. These effects are time dependent. Celastrol also inhibits Hsp90 and thereby accentuates the radio sensitivity of pulmonary malignancies (Lee et al., 2011). As a result increased p53 expression is also seen.
机译：王et al。[2012]提供了有趣的数据在他们最近的文章。施加重大anti-neoplastic效应其他系统的恶性肿瘤。celastrol抑制肿瘤生长在乳房恶性肿瘤。在癌变NF-KB-mediated MMP-9表达式细胞(Kim et al ., 2011)。肿瘤侵袭性以及变弱转移。从而进一步减少肿瘤的生长。增殖抑制调制的一个线粒体相关的半胱天冬酶通路。水平通常是上调(杨et al。201我)。另一方面,bcl - 2水平下降了监管。这些变化,进一步增强肿瘤的生长抑制。调节雌激素受体从而进一步抑制肿瘤的生长。黑帮receptor抄写了et al .,2011)。细胞肺癌癌。激活FasL介导的细胞凋亡。同时,它也引起线粒体介导的癌细胞凋亡。膜电位明显减弱。同时,减少bcl - 2表达同时增加肿瘤内伯灵顿的表情细胞(谅解备忘录et al ., 201)。Caspase-3乳沟也增强导致进一步增强细胞凋亡。Celastrol从而也抑制了一半强调了收音机的敏感性肺恶性肿瘤(Lee et al ., 2011)。增加p53表达也见过。

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