PKC?-dependent activation of the ubiquitin proteasome system is responsible for high glucose-induced human breast cancer MCF-7 cell proliferation, migration and invasion.

PKC?-dependent activation of the ubiquitin proteasome system is responsible for high glucose-induced human breast cancer MCF-7 cell proliferation, migration and invasion.
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PKC? 依赖性泛素蛋白酶体系统激活是高糖诱导人乳腺癌 MCF-7 细胞增殖、迁移和侵袭的原因。

DOI:
10.7314/apjcp.2013.14.10.5687
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发表时间:
2013-10
期刊:
Asian Pac J Cancer Prev
影响因子:
--
通讯作者:
Sun, Sheng-Rong
Sun, Sheng-Rong
中科院分区:
其他
文献类型:
--
作者:
Tang, Zhao;Khan, Shahzad;Wang, Chang-Hua;Sun, Sheng-Rong

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2型糖尿病(T2DM)在过去几十年中促进了晚期乳腺癌的发展。然而,这种促进作用背后的机制却鲜为人知。在这项研究中,我们确定高血糖增强了蛋白酶体活性(最后一个单词“activ”似乎不完整,可能是“activity”)
Type 2 diabetes mellitus (T2DM) has contributed to advanced breast cancer development over the past decades. However, the mechanism underlying this contribution is poorly understood. In this study, we determined that high glucose enhanced proteasome activity was accompanied by enhanced proliferation, migration and invasion, as well as suppressed apoptosis, in human breast cancer MCF-7 cells. Proteasome inhibitor bortezomib (BZM) pretreatment mitigated high glucose-induced MCF-7 cell growth and invasion. Furthermore, high glucose increased protein kinase C delta (PKC?)-phosphorylation. Administration of the specific PKC? inhibitor rottlerin attenuated high glucose-stimulated cancer cell growth and invasion. In addition, PKC? inhibition by both rottlerin and PKC? shRNA significantly suppressed high glucose-induced proteasome activity. Our results suggest that PKC?-dependent ubiquitin proteasome system activation plays an important role in high glucose- induced breast cancer cell growth and metastasis.
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