Ling-di Ma1,2, Gui-Bin Lin3, Lu-Bo Yang4, Jia-Lin Cao3, Jian Wang4, Qiong-di Chen4, Wei-Qiang Li4, Wang-Jing Zhong3. 1. Laboratory Center, the Third People's Hospital of Huizhou, Affiliated Hospital of Guangzhou Medical University, Huizhou, Guangdong Province, 516002, China. lingdimawsh@126.com. 2. Clinical Laboratory, the Third People's Hospital of Huizhou, Affiliated Hospital of Guangzhou Medical University, Huizhou, Guangdong Province, 516002, China. lingdimawsh@126.com. 3. Laboratory Center, the Third People's Hospital of Huizhou, Affiliated Hospital of Guangzhou Medical University, Huizhou, Guangdong Province, 516002, China. 4. Clinical Laboratory, the Third People's Hospital of Huizhou, Affiliated Hospital of Guangzhou Medical University, Huizhou, Guangdong Province, 516002, China.
Abstract
OBJECTIVE: To study the mechanism of the anti-tumor effect of Morinda citrifolia (noni). METHODS: The influences of noni juice on cell proliferation, apoptosis, invasion, migration and the activity of AKT/nuclear factor- κ B (NF- κ B) signaling pathway in A549 human lung cancer cells were detected by MTT, cell counting kit-8, colony formation, Annexin V/PI double labeling, transwell, scratch test and immunoblotting assay, respectively. A549 cells were inoculated into the right axilla of nude mice, followed by noni juice treatment. The body weight of the nude mice was weighed, and the tumor volume and weight were measured. Cell proliferation and expression of apoptosis-related proteins were measured by immunohistochemistry, and the activity of NF- κ B signaling pathway was measured by immunoblotting. RESULTS: The in vitro studies showed that noni juice inhibited the A549 cells proliferation, migration and invasion. Noni juice also promoted cells apoptosis in A549 cells. Immunoblotting assay showed that the phosphorylation level of AKT, p50, and STAT3 proteins was inhibited to different extents after noni juice treatment. The in vivo studies showed that noni juice effectively suppressed tumor formation of A549 cells in nude mice. Noni juice treatment inhibited the expression of Ki67, PCNA, and Bcl-2 protein in the tumor; while promoted the expression of caspase-3 protein. Additionally, we also found that noni juice treatment could restrain the activity of AKT/NF- κ B signaling pathway in the tumor tissue. CONCLUSION: Noni juice inhibited the proliferation of A549 lung cancer cells, induced apoptosis, and inhibited cell invasion and migration via regulating AKT/NF- κ B signaling pathway.
OBJECTIVE: To study the mechanism of the anti-tumor effect of Morinda citrifolia (noni). METHODS: The influences of noni juice on cell proliferation, apoptosis, invasion, migration and the activity of AKT/nuclear factor- κ B (NF- κ B) signaling pathway in A549 human lung cancer cells were detected by MTT, cell counting kit-8, colony formation, Annexin V/PI double labeling, transwell, scratch test and immunoblotting assay, respectively. A549 cells were inoculated into the right axilla of nude mice, followed by noni juice treatment. The body weight of the nude mice was weighed, and the tumor volume and weight were measured. Cell proliferation and expression of apoptosis-related proteins were measured by immunohistochemistry, and the activity of NF- κ B signaling pathway was measured by immunoblotting. RESULTS: The in vitro studies showed that noni juice inhibited the A549 cells proliferation, migration and invasion. Noni juice also promoted cells apoptosis in A549 cells. Immunoblotting assay showed that the phosphorylation level of AKT, p50, and STAT3 proteins was inhibited to different extents after noni juice treatment. The in vivo studies showed that noni juice effectively suppressed tumor formation of A549 cells in nude mice. Noni juice treatment inhibited the expression of Ki67, PCNA, and Bcl-2 protein in the tumor; while promoted the expression of caspase-3 protein. Additionally, we also found that noni juice treatment could restrain the activity of AKT/NF- κ B signaling pathway in the tumor tissue. CONCLUSION: Noni juice inhibited the proliferation of A549 lung cancer cells, induced apoptosis, and inhibited cell invasion and migration via regulating AKT/NF- κ B signaling pathway.