Background Breast cancer is the leading cause of cancer-related death in women worldwide. Although traditional Chinese medicine (TCM) is commonly used by patients with breast cancer, little is known about TCM prescriptions for breast cancer. This study investigated the effects of a new TCM formula, T33, comprising Radix Kansui , Rheum rhabarbarum , Paeonia lactiflora , Jiangbanxia , and Zhigancao on breast cancer cells in vitro and in vivo. Methods To evaluate the effects of T33 on human breast cancer, HMEpiC, MDA-MB231 and MCF-7 cells were treated with different concentrations of T33 and then analyzed using MTT and Transwell migration assays. To elucidate the involvement of autophagy in the T33-induced death of MDA-MB231 and MCF-7 cells, immunofluorescence staining with LC3-II-specific antibodies was performed. Tumor xenografts were generated by subcutaneously injecting either MDA-MB231 or MCF-7 cells into BALB/c nude mice to determine the effects of T33 on these cell lines in vivo. Results The experimental results revealed that 0.1 mg/mL, 0.5 mg/mL, 2.5 mg/mL, 5 mg/mL and 10 mg/mL T33 significantly inhibited the proliferation and invasion of MDA-MB231 and MCF-7 cells. Moreover, significant autophagy was observed in MDA-MB231 and MCF-7 cells in the presence of 2.5 mg/mL, 5 mg/mL and 10 mg/mL T33. An animal study further revealed that both low (200 mg/kg) and high (600 mg/kg) doses of T33 inhibited the proliferation of xenografted breast cancer cells in BALB/c nude mice. Conclusion These findings demonstrate for the first time that T33 has potential in the treatment of breast cancer owing to its antiproliferative effects and induction of autophagy.
Colorectal cancer (CRC) is a leading cause of cancer-related death globally. Although surgery is still the major method for CRC therapy, the adoption of alternative treatments, such as traditional Chinese medicine (TCM), for CRC treatment is increasing.Our previous study has indicated the anti-breast cancer activity of T33 (a TCM formula). Interestingly, a major ingredient in T33, Baishao (Paeoniae Radix Alba), was reported to have antiproliferative effects on CRC cells. Therefore, this study further validated the influences of T33 on HT-29 and Caco2 cells both in vitro and in vivo. Viability and migration assays were performed to analyze the influences of T33 on proliferation and migratory activity of HT-29 and Caco2 cells. Immunofluorescence (IF) staining and immunoblotting were performed to confirm T33-induced autophagy in HT-29 and Caco2 cells. Xenograft HT-29 tumors were generated to test the effects of T33 in vivo. Significantly reduced survival and migratory activity were observed in both HT-29 and Caco2 cells treated with T33 along with apparently increased LC3-II protein. Significantly decreased p62/SQSTM1 protein, increased LC3-II/LC3-I ratio, and elevated amounts of Atg7, Atg5, and Beclin-1 proteins were detected in both HT-29 and Caco2 cells treated with T33. Moreover, the volume of xenograft HT-29 tumors was significantly lower in mice receiving 200 or 600 mg/ kg T33 than in control-treated mice. These findings indicate that T33 exerts anti-CRC activity by inducing autophagy and suggest the potential of T33 for CRC treatment.
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