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

Neoplasma 2018 September 17
Colorectal cancer (CRC) is a common malignant tumor with the high increase and mortality worldwide. Skullcapflavone I has been reported to exert anti-tumor effect in several cancers. Recent studies demonstrated that microRNA-107 and tropomyosin alpha-1 (TPM1) are important regulator in cell proliferation of different cancer cells. However, the role of Skullcapflavone I in CRC has not been investigated. Moreover, whether miR-107 and TPM1 are involved in regulating the effect of Skullcapflavone on CRC cells remains unclear. In the study, we aimed to explore the effects of Skullcapflavone I on CRC cells proliferation, and to uncover the regulatory effect of miR-107 and TPM1 on this process. The results showed that Skullcapflavone I significantly suppressed cell proliferation, viability and down-regulated the protein levels of PCNA and Cyclin D1. The expression of miR-107 was down-regulated by Skullcapflavone I, and overexpression of miR-107 abolished the anti-proliferative effect of Skullcapflavone I. In addition, we found that Skullcapflavone I remarkably promoted TPM1 expression by down-regulation of miR-107. Furthermore, Skullcapflavone I inhibited the activations of MEK/ERK and NF-κB signal pathways by regulation of TPM1in HCT116 cells. These results demonstrated that Skullcapflavone I increased the expression of TPM1 by down-regulating miR-107, and inhibiting MEK/ERK and NF-κB signal pathways, and eventually inhibited cell proliferation of HCT116 cells. These finding may provide a new method for the treatment of CRC.

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