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Curcumin inhibits lung cancer cell invasion and metastasis through the tumor suppressor HLJ1

机译：Curcumin inhibits lung cancer cell invasion and metastasis through the tumor suppressor HLJ1

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Curcumin (diferuloylmethane) is an active component of the spice turmeric and has a diversity of antitumor activities. In this study, we found that curcumin can inhibit cancer cell invasion and metastasis through activation of the tumor suppressor DnaJ-like heat shock protein 40 (HLJ1). Human lung adenocarcinoma cells (CL1-5) treated with curcumin (1-20 mu mol/L) showed a concentration-dependent reduction in cell migration, invasion, and metastatic ability, and this was associated with increased HLJ1 expression. Knockdown of HLJ1 expression by siRNA was able to reverse the curcumin-induced anti-invasive and antimetastasis effects in vitro and in vivo. The HLJ1 promoter and enhancer in a luciferase reporter assay revealed that curcumin transcriptionally up-regulates HLJ1 expression through an activator protein (AP-1) site within the HLJ1 enhancer. junD, one of the AP-1 components, was significantly up-regulated by curcumin (1-20 mu mol/L) in a concentration- and time-dependent manner. Knockdown of junD expression could partially reduce the curcumin-induced HLJ1 activation and diminish the anti-invasive effect of curcumin, indicating that junD would seem to be involved in curcumin-induced HLJ1 expression. Curcumin was able to induce c-Jun NH2-kinase (JNK) phosphorylation, whereas the JNK inhibitor (SP-600125) could attenuate curcumin-induced JunD and HLJ1 expression. Activation of HLJ1 by curcumin further leads to up-regulation of E-cadherin and a suppression of cancer cell invasion. Our results show that curcumin induces HLJ1, through activation of the JNK/JunD pathway, and inhibits lung cancer cell invasion and metastasis by modulating E-cadherin expression. This is a novel mechanism and supports the application of curcumin in anti-cancer metastasis therapy.
机译：姜黄素（二氟甲酰甲烷）是香料姜黄的活性成分，具有多种抗肿瘤活性。在这项研究中，我们发现姜黄素可通过激活抑癌DnaJ样热激蛋白40（HLJ1）来抑制癌细胞的侵袭和转移。姜黄素（1-20μmol/ L）处理的人肺腺癌细胞（CL1-5）在细胞迁移，侵袭和转移能力方面呈浓度依赖性降低，这与HLJ1表达增加有关。 siRNA抑制HLJ1表达能够在体外和体内逆转姜黄素诱导的抗侵袭和抗转移作用。萤光素酶报告基因测定中的HLJ1启动子和增强子显示姜黄素通过HLJ1增强子内的激活蛋白（AP-1）位点转录上调HLJ1表达。姜黄素（1-20μmol/ L）以浓度和时间依赖性方式显着上调了AP-1成分之一junD。剔除junD表达可部分减少姜黄素诱导的HLJ1活化并减弱姜黄素的抗侵袭作用，表明junD似乎与姜黄素诱导的HLJ1表达有关。姜黄素能够诱导c-Jun NH2-激酶（JNK）磷酸化，而JNK抑制剂（SP-600125）可以减弱姜黄素诱导的JunD和HLJ1表达。姜黄素激活HLJ1进一步导致E-钙粘蛋白上调并抑制癌细胞侵袭。我们的结果表明姜黄素通过激活JNK / JunD途径诱导HLJ1，并通过调节E-钙黏着蛋白表达抑制肺癌细胞的侵袭和转移。这是一种新颖的机制，支持姜黄素在抗癌转移治疗中的应用。

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