Kim Mi-Sung, Lim Do Young, Kim Jong-Eun, Chen Hanyong, Lubet Ronald A, Dong Zigang, Bode Ann M
The Hormel Institute, University of Minnesota, Minneapolis, Minnesota.
Chemoprevention Agent Development Research Group, Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland.
Mol Carcinog. 2015 Dec;54(12):1596-604. doi: 10.1002/mc.22232. Epub 2014 Oct 18.
9-cis-UAB30 (UAB30) and Targretin are well-known retinoid X receptor (RXR) agonists. They were highly effective in decreasing the incidence of methylnitrosourea (MNU)-induced mammary cancers. However, whether the anti-mammary cancer effects of UAB30 or Targretin originate from the activation of RXR is unclear. In the present study, we hypothesized that UAB30 and Targretin not only affect RXR, but likely influence one or more off-target proteins. Virtual screening results suggest that Src is a potential target for UAB30 and Targretin that regulates extracellular matrix (ECM) molecules and cell motility and invasiveness. In vitro kinase assay data revealed that UAB30 or Targretin interacted with Src and attenuated its kinase activity. We found that UAB30 or Targretin substantially inhibited invasiveness and migration of MCF-7 and SK-BR-3 human breast cancer cells. We examined the effects of UAB30 and Targretin on the expression of matrix metalloproteinases (MMP)-9, which are known to play an essential role in tumor invasion. We show that activity and expression of MMP-9 were decreased by UAB30 or Targretin. Western blot data showed that UAB30 or Targretin decreased AKT and its substrate molecule p70(s6k), which are downstream of Src in MCF-7 and SK-BR-3 cells. Moreover, knocking down the expression of Src effectively reduced the sensitivity of SK-BR-3 cells to the inhibitory effects of UAB30 and Targretin on invasiveness. Taken together, our results demonstrate that UAB30 and Targretin each inhibit invasion and migration by targeting Src in human breast cancer cells.
9-顺式维甲酸UAB30(UAB30)和他扎罗汀是著名的维甲酸X受体(RXR)激动剂。它们在降低甲基亚硝基脲(MNU)诱导的乳腺癌发病率方面非常有效。然而,UAB30或他扎罗汀的抗乳腺癌作用是否源于RXR的激活尚不清楚。在本研究中,我们假设UAB30和他扎罗汀不仅影响RXR,而且可能影响一种或多种脱靶蛋白。虚拟筛选结果表明,Src是UAB30和他扎罗汀的潜在靶点,可调节细胞外基质(ECM)分子以及细胞的运动性和侵袭性。体外激酶分析数据显示,UAB30或他扎罗汀与Src相互作用并减弱其激酶活性。我们发现UAB30或他扎罗汀可显著抑制MCF-7和SK-BR-3人乳腺癌细胞的侵袭性和迁移。我们研究了UAB30和他扎罗汀对基质金属蛋白酶(MMP)-9表达的影响,已知MMP-9在肿瘤侵袭中起重要作用。我们发现UAB30或他扎罗汀可降低MMP-9的活性和表达。蛋白质印迹数据显示,UAB30或他扎罗汀可降低MCF-7和SK-BR-3细胞中Src下游的AKT及其底物分子p70(s6k)。此外,敲低Src的表达可有效降低SK-BR-3细胞对UAB30和他扎罗汀侵袭抑制作用的敏感性。综上所述,我们的结果表明,UAB30和他扎罗汀均通过靶向人乳腺癌细胞中的Src来抑制侵袭和迁移。