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Herbal medicine teng-long-bu-zhong-tang inhibits the growth of human RKO colorectal cancer by regulating apoptosis, senescence, and angiogenesis
Meng-Meng Wei1, Shuang-Shuang Wang2, Jia-Lu Zheng3, Lei Chen4, Xiao Peng4, Jin-Fang Chen4, Hong-Mei An5, Bing Hu4
1 Institute of Traditional Chinese Medicine in Oncology; Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai; Out-patient Department, Pingdu Hospital of Traditional Chinese Medicine, Shandong, China
2 Institute of Traditional Chinese Medicine in Oncology; Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai; Student Affairs Department, Shanghai University of Traditional Chinese Medicine, Shanghai, China
3 Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
4 Institute of Traditional Chinese Medicine in Oncology; Department of Oncology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
5 Department of Science and Technology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
Correspondence Address:
Dr. Bing Hu
725 South Wanping Rd., Shanghai 200032
China
 Source of Support: None, Conflict of Interest: None  | 5 |
DOI: 10.4103/wjtcm.wjtcm_42_21
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Background: Teng-Long-Bu-Zhong-Tang (TLBZT) is a traditional Chinese herbal medicine used to treat colorectal cancer (CRC). In the present study, we observed the anti-cancer effects of TLBZT on human RKO CRC. Materials and Methods: Mice were subcutaneously transplanted with RKO cells, divided into control, 5-Fu-administered, TLBZT-administered, and TLBZT and 5-Fu combination-administered groups, and treated with 5-Fluorouracil (5-Fu) and/or TLBZT. Apoptosis was detected by TdT-mediated dUTP nick-end labeling assay. The activity of caspase-3,-8, and-9 was detected using specific commercial kits. Cell senescence was assessed using senescence β-galactosidase staining. Protein expression was evaluated by immunohistochemistry. Results: TLBZT inhibited RKO CRC tumor growth, enhanced the anti-cancer effects of 5-Fu, induced apoptosis, and activated caspase-3,-8, and-9. TLBZT induced cell senescence accompanied by the downregulation of cyclin E1 and cyclin-dependent kinase 2 expressions. TLBZT also inhibited angiogenesis and the expression of hypoxia-inducible factor 1 subunit alpha and vascular endothelial growth factor-A. Conclusions: TLBZT inhibited RKO CRC tumor growth and enhanced the anti-cancer effects of 5-Fu, and it could be associated with apoptosis and cell senescence induction, and angiogenesis inhibition.
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