Enhancer of zeste homolog 2 (EZH2), an oncogene, is a commonly up‐regulated epigenetic factor in human cancer. Hepatocellular carcinoma deletion gene 1 (DLC1) is an antioncogene that is either expressed at low levels or not expressed in many malignant tumours. Curcumin is a promising anticancer drug that has antitumour effects in many tumours, but its mechanism of action is unclear. Our research demonstrated that EZH2 was up‐regulated in breast cancer (BC) tissues and cells, whereas DLC1 was down‐regulated, and the expression of EZH2 and DLC1 was negatively correlated in BC. By analysing the characteristics of clinical cases, we found that positive expression of EZH2 and negative expression of DLC1 may be predictors of poor prognosis in patients with triple‐negative breast cancer (TNBC). Moreover, knockdown of EZH2 expression restored the expression of DLC1 and inhibited the migration, invasion and proliferation, promoted the apoptosis, and blocked the cell cycle of MDA‐MB‐231 cells. Furthermore, we found that curcumin restored the expression of DLC1 by inhibiting EZH2; it also inhibited the migration, invasion and proliferation of MDA‐MB‐231 cells, promoted their apoptosis and blocked the cell cycle. Finally, xenograft tumour models were used to demonstrate that curcumin restored DLC1 expression by inhibiting EZH2 and also inhibited the growth and promoted the apoptosis of TNBC cells. In conclusion, our results suggest that curcumin can inhibit the migration, invasion and proliferation, promote the apoptosis, block the cycle of TNBC cells and restore the expression of DLC1 by inhibiting the expression of EZH2.

中文翻译：

---

姜黄素通过沉默EZH2和恢复DLC1表达来抑制三阴性乳腺癌细胞的生长。

Zeste同源基因2（EZH2）的增强子，一种癌基因，是人类癌症中通常被上调的表观遗传因子。肝细胞癌缺失基因1（DLC1）是一种抑癌基因，其表达水平低或在许多恶性肿瘤中均不表达。姜黄素是一种有前途的抗癌药物，在许多肿瘤中均具有抗肿瘤作用，但其作用机理尚不清楚。我们的研究表明，EZH2在乳腺癌（BC）组织和细胞中被上调，而DLC1被下调，并且EZH2和DLC1在BC中的表达呈负相关。通过分析临床病例的特征，我们发现EZH2阳性表达和DLC1阴性表达可能是三阴性乳腺癌（TNBC）患者预后不良的预测指标。此外，抑制EZH2表达可恢复DLC1的表达并抑制迁移，侵袭和增殖，促进细胞凋亡，并阻断MDA-MB-231细胞的细胞周期。此外，我们发现姜黄素通过抑制EZH2恢复了DLC1的表达。它也抑制了MDA-MB-231细胞的迁移，侵袭和增殖，促进了它们的凋亡并阻断了细胞周期。最后，异种移植肿瘤模型被用来证明姜黄素通过抑制EZH2恢复了DLC1表达，还抑制了TNBC细胞的生长并促进了其凋亡。总之，我们的结果表明姜黄素可以通过抑制EZH2的表达来抑制迁移，侵袭和增殖，促进细胞凋亡，阻断TNBC细胞的周期并恢复DLC1的表达。