Skullcapflavone I inhibits proliferation of human colorectal cancer cells via down-regulation of miR-107 expression

被引:19
作者
Zhang, W. [1 ]
Li, W. [1 ]
Han, X. [1 ]
机构
[1] Shengli Oilfield Cent Hosp, Dept Gastroenterol, Dongying, Peoples R China
关键词
Skullcapflavone I; proliferation; microRNA-107; TPM1; MEK/ERK; NF-kappa B; SCUTELLARIA-BAICALENSIS; PROMOTES PROLIFERATION; GENE-EXPRESSION; BREAST-CANCER; APOPTOSIS; VITRO; PROGRESSION; MICRORNA; GROWTH; INJURY;
D O I
10.4149/neo_2018_180427N279
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Colorectal cancer (CRC) is a common malignant tumor with high global increase and mortality. While Skullcapflavone I has been reported to exert anti-tumor effect in several cancers, its role in CRC has not previously been investigated. Recent studies have also demonstrated that microRNA-107 (miR-107) and tropomyosin alpha-1 (TPM1) are important regulators of cancer cell proliferation, but it remains unclear if these are involved in regulating the effect of Skullcapflavone I on CRC cells. This study therefore assessed the effects of Skullcapflavone I on CRC cell proliferation and investigated miR-107 and TPM1 regulatory effects on this process. The results showed that Skullcapflavone I significantly suppressed cell proliferation and viability and down-regulated PCNA and Cyclin Diprotein levels. It also down-regulated miR-107 expression which then promoted TPM1 expression, but miR-107 over-expression abolished Skullcapflavone I anti-proliferative effects. Furthermore, Skullcapflavone I inhibited the activations of MEK/ERK and NF-kappa B signal pathway activation by regulating TPM1 in HCT116 cells. These results demonstrated that Skullcapflavone I increased the expression of TPM1 by downregulating miR-107 and inhibiting the MEK/ERK and NF-kappa B signal pathways. It then inhibited HCT116 cell proliferation, and therefore Skullcapflavone I may provide new methodology in colorectal cancer treatment.
引用
收藏
页码:203 / 210
页数:8
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