This study tested the hypothesis that heparanase (HPSE) is related to tumor metastasis and curcumin (CCM) inhibits tumor metastasis by down‐regulating HPSE expression. MTT, Transwell assays, and RT‐PCR were used to study the effects of CCM on the migration and invasion of CT26 cells and the expression of HPSE. CT26 cells were transfected with lentivirus to establish HPSE‐overexpressing cells (OE) and corresponding negative control cells (NC). Signal pathways involved in down‐regulating the expression of HPSE and inhibiting the migration and invasion of CT26 cells by CCM were screened by the liquid crystal chip. HPSE promoted CT26 cells migration and invasion, and CCM inhibited the proliferation and metastasis of CT26 cells. The results of RT‐PCR indicated that CCM down‐regulated HPSE expression. Liquid phase microarray showed that CCM inhibited the phosphorylation of P38 and STAT5 in CT26 cells and NC cells. In contrast, the inhibitory function of CCM was markedly enhanced when HPSE was overexpressed (P < 0.05). In short, HPSE is closely related to metastasis of colon cancer cells. CCM inhibits colon cancer cell migration and invasion by inhibiting HPSE expression, which may be related to P38 MAPK and JAK/STAT5 signal pathways.

中文翻译：

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姜黄素通过降低乙酰肝素酶表达来抑制CT26细胞转移。

这项研究验证了乙酰肝素酶（HPSE）与肿瘤转移有关，姜黄素（CCM）通过下调HPSE表达抑制肿瘤转移的假设。使用MTT，Transwell分析和RT-PCR研究了CCM对CT26细胞迁移和侵袭以及HPSE表达的影响。用慢病毒转染CT26细胞，以建立HPSE过表达细胞（OE）和相应的阴性对照细胞（NC）。液晶芯片筛选了与下调HPSE表达，抑制CCM抑制CT26细胞迁移和侵袭有关的信号通路。HPSE促进CT26细胞的迁移和侵袭，而CCM抑制CT26细胞的增殖和转移。RT-PCR结果表明CCM下调了HPSE表达。液相微阵列显示CCM抑制CT26细胞和NC细胞中P38和STAT5的磷酸化。相反，当HPSE过表达时，CCM的抑制功能显着增强（P  <0.05）。简而言之，HPSE与结肠癌细胞的转移密切相关。CCM通过抑制HPSE表达来抑制结肠癌细胞的迁移和侵袭，这可能与P38 MAPK和JAK / STAT5信号通路有关。