High glucose promotes breast cancer proliferation and metastasis by impairing angiotensinogen expression
High glucose promotes breast cancer proliferation and metastasis by impairing angiotensinogen expression
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DOI：
10.1042/bsr20190436
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发表时间：
2019-06-14
影响因子：
4
通讯作者：
Bai, Lei
中科院分区：
文献类型：
--
作者：
Sun, Shichao;Sun, Yao;Bai, Lei
许多研究都指出了高血糖在乳腺癌中的重要性，然而，血管紧张素原(AGT)在这一场景中的作用尚未确定。在这里，我们开始分析高糖在乳腺癌中的潜在促肿瘤作用，并了解其潜在的分子机制。我们证明了高糖促进了乳腺癌细胞的增殖、活性和非锚定生长。此外，高糖培养可显著增强细胞的迁移能力和侵袭能力。从机制上讲，高糖在转录和翻译水平上都抑制了AGT的表达。高AGT显著抑制乳腺癌细胞的增殖，抑制其活力，并抑制其迁移/侵袭。最重要的是，异位引入AGT几乎完全消除了高糖的促肿瘤作用。我们的研究描述了高糖在乳腺癌细胞中的促肿瘤特性，这主要归因于对AGT的抑制。
A number of investigations have addressed the importance of high glucose in breast cancer, however, the involvement of angiotensinogen (AGT) in this scenario is yet to be defined. Here we set out to analyze the potential pro-tumor effects of high glucose in breast cancer, and understand the underlying molecular mechanism. We demonstrated that high glucose promoted cell proliferation, viability, and anchorage-independent growth of breast cancer cells. In addition, the migrative and invasive capacities were significantly enhanced by high glucose medium. Mechanistically, AGT expression was inhibited by high glucose at both transcriptional and translational levels. High AGT remarkably suppressed proliferation, inhibited viability, and compromised migration/invasion of breast cancer cells. Most importantly, ectopic introduction of AGT almost completely abrogated pro-tumor effects of high glucose. Our study has characterized the pro-tumor properties of high glucose in breast cancer cells, which is predominantly attributed to the suppression of AGT.