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Curcumin inhibits CT26 cells metastasis by decreasing heparanase expression
Author(s) -
Li Shanshan,
Fu Hui,
Wang Yiyang,
Wang Li,
Jia Beitian,
Bian Yuhong
Publication year - 2020
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.1ma0620-357r
Subject(s) - heparanase , metastasis , cancer research , biology , cancer cell , cell migration , curcumin , transfection , p38 mitogen activated protein kinases , mapk/erk pathway , microbiology and biotechnology , cell , signal transduction , cancer , cell culture , pharmacology , biochemistry , genetics
Abstract 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.