J Cancer 2022; 13(3):847-857. doi:10.7150/jca.66177 This issue Cite
Research Paper
1. Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China
2. Department of Biochemistry & Molecular Biology, Metabolic Disease Research Center, School of Basic Medicine, Anhui Medical University, Hefei, 230032, China
3. Anhui Provincial Institute of Translational Medicine, Hefei, 230022, China
4. Department of General Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China
5. The First Clinical Medical College of Anhui Medical University, Hefei 230032, China
6. Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China
7. Department of Gastrointestinal Surgery, General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China
8. School of Pharmacy, Anhui Medical University, Hefei, 230032, China
*These authors have contributed equally.
Colorectal cancer (CRC) is a malignant disease that is a serious threat to human health. Rutaecarpine (RUT) is an important bioactive alkaloid of Evodia rutaecarpa. According to previous studies, RUT suppressed the proliferation of several human tumors. However, its role in colorectal tumorigenesis remained unknown. The aim of the present study was to determine the functions of RUT in CRC. Here, we have demonstrated that RUT inhibited the proliferation, migration and invasion of CRC cells in vitro. Further, RUT was found to induce the apoptosis of CRC cells. Mechanistically, RUT decreased the phosphorylation levels of NF-κB and STAT3. Moreover, treatment with RUT upregulated the expression of cleaved-Caspase3 and downregulated the expression of Bcl-2 in CRC. In addition, our findings suggested that RUT inhibited the growth and lung metastasis of CRC Cells in vivo. Based on immunofluorescence analysis, the expression of Ki67 was downregulated while that of cleaved-Caspase3 was upregulated in RUT-treated tumors compared with control-treated tumors. Taken together, our findings indicate that RUT can inhibit the proliferation and migration of CRC cells, and induce the apoptosis of CRC cells by inactivating NF-κB/STAT3 signaling. Our study highlights the potential clinical application of RUT for the treatment of CRC.
Keywords: colorectal cancer, Rutaecarpine, STAT3, NF-κB, proliferation, apoptosis