ABSTRACT
Malignant tumors are major chronic diseases that threaten human health worldwide and one of the most serious public health problems in China and even in the world in the 21st century. How to effectively control and even cure tumors is also one of the most essential problems in the medical field today. Currently, although surgery, chemotherapy and radiotherapy remain the main therapies, the accompanying adverse events of chemotherapy and radiotherapy cannot be ignored. Therefore, it is of great significance to find new anti-tumor targeted drugs with a low toxicity and strong effects. Capsaicin is a plant base of fat-soluble vanillin amide isolated from Solanaceae. Its chemical structure is trans-8-methyl-N-vanillyl-6-nonenamide (C18H27NO3), a type of monoclinic rectangular flake of colorless crystals, which is the main biologically active ingredient in peppers. Capsaicin has a wide range of pharmacological effects, including anti-oxidation, prevention of cardiovascular disease, protection of gastrointestinal mucosa, analgesia, anti-inflammation, itching relief and even anti-tumor. Numerous studies indicated that capsaicin has significant anti-tumor effects in vivo and in vitro. Capsaicin can play a chemopreventive role by regulating the metabolism of carcinogens and the interaction of carcinogens with DNA. As well, capsaicin was proven to play an anti-tumor effect by inhibiting tumor cell proliferation, inducing tumor cell cycle arrest, promoting tumor cell apoptosis, inhibiting tumor cell migration, invasion and metastasis, inhibiting tumor angiogenesis, regulating tumor cell autophagy and mediating of tumor immunity. In this paper, we searched, analyzed, and summarized domestic and foreign literatures relating to capsaicin in recent years. We reviewed the effect of capsaicin on inhibiting tumor cell proliferation, inducing tumor cell cycle arrest, promoting tumor cell apoptosis, inhibiting tumor cell migration, invasion and metastasis, inhibiting tumor angiogenesis, regulating tumor cell autophagy and mediating of tumor immunity, as well as the underlying main molecular mechanisms, so as to provide scientific and theoretical basis for further research, development and utilization of capsaicin.
ABSTRACT
Objective: To investigate the effect of capsaicin on the migration and invasion of human breast cancer MCF-7 cells and the underlying molecular mechanism. Method: Three capsaicin intervention groups of different concentrations (25, 50, 75 μmol·L-1) and a blank group were set up. After MCF-7 cells were treated with different concentrations of capsaicin (25, 50, 75 μmol·L-1) for 24 h, the cell migration and invasion abilities were assessed by Transwell migration and invasion assay, respectively. Meanwhile, the mRNA level of silent information regulator 2 homolog 1 (SIRT1) and DNA polymerase δ catalytic subunit p125 encoding gene POLD1 (POLD1) were detected by Real-time polymerase chain reaction (Real-time PCR). The protein levels of SIRT1 and DNA polymerase δ catalytic subunit p125 (p125) were detected by Western blot. Result: Compared with the blank group, the number of transmembrane cells was significantly reduced, and the mobility was significantly decreased (P-1) in MCF-7 cells for 24 h. Capsaicin (25, 50, 75 μmol·L-1) significantly down-regulated the mRNA and protein expressions of SIRT1 (P-1) in MCF-7 cells for 24 h. Furthermore, capsaicin (25, 50, 75 μmol·L-1) also significantly down-regulated the mRNA expression of POLD1 and the protein expression of p125 (P-1) in MCF-7 cells for 24 h. Conclusion: Capsaicin remarkably inhibits the cell migration and invasion of breast cancer MCF-7 cells, and the possible mechanism may be related to the down-regulation of SIRT1 and POLD1 mRNA expression levels and SIRT1 and p125 protein expression levels.
ABSTRACT
Objective: To investigate the inhibitory effect of capsaicin on the growth of breast cancer MDA-MB-231 cells transplanted tumour in nude mice and its possible molecular mechanism. Method: Transplanted tumor model of breast cancer MDA-MB-231 cells in nude mice were established. Then the tumor-bearing mice were randomly divided into 4 groups:model group, and low, medium and high-dose capsaicin groups (5, 10, 20 mg·kg-1). Mice of low, medium and high-dose capsaicin groups (5, 10, 20 mg·kg-1) were intraperitoneally injected with the corresponding dose of capsaicin, and the model group was injected with the same volume of phosphate buffer saline (PBS), once every 3 days, for a total of 8 times in succession. Body weight of mice and transplantation tumor volume were measured before each injection of capsaicin. Mice of each group were put to death 24 h after the last administration, and then the tumor volume, mass and the tumor inhibitory rate were calculated. The protein expression levels of high mobility group box 1 (HMGB1) and Toll-like receptors 4(TLR4) were measured by immunohistochemistry and Western blot. Result: No significant difference was observed between each group in body weight. However, compared with the model group, capsaicin (5, 10, 20 mg·kg-1) remarkably inhibited the tumor volume and mass (PPP-1) also markedly inhibited the protein expression levels of HMGB1 and TLR4 (PConclusion: Capsaicin remarkably inhibits the growth of breast cancer MDA-MB-231 cells transplanted tumour in nude mice, and the possible mechanism may be related to the down-regulation of HMGB1 and TLR4 at the protein level.
ABSTRACT
This work aimed to observe the effects of short hairpin RNA (shRNA)-silenced FBI-1 (factor that binds to the inducer of short transcripts of human immunodeficiency virus-1) on proliferation and apoptosis of triple-negative breast cancer cell line MDA-MB-231. qRT-PCR and Western blot analysis were applied to detect the mRNA and/or protein expression of FBI-1, Bcl-2, Bax, cleaved-Caspase 3 and Survivin. RNA interference method was used to silence FBI-1 expression in MDA-MB-231 cells. CCK-8 and colony formation assay were employed to detect the cell proliferation. Flow cytometry was employed for examining cell apoptosis. In vivo tumorigenicity of MDA-MB-231 cells was detected by tumor transplantation in nude mice. The results showed that the mRNA and protein expressions of FBI-1 were higher in MDA-MB-231 cells compared with those in normal human mammary epithelial cells MCF-10A. FBI-1 gene silencing inhibited proliferation and induced apoptosis of MDA-MB-231 cells in vitro, together with decreased Bcl-2 and Survivin protein expression, increased Bax protein expression and activated Caspase 3. Moreover, FBI-1 gene silencing inhibited the tumorigenesis of MDA-MB-231 cells in vivo. These results suggest that silencing of FBI-1 gene inhibits proliferation, induces apoptosis and suppresses the tumorigenesis of MDA-MB-231 cells.