We previously reported that caffeine-assisted chemotherapy improved the treatment of malignant bone and soft tissue tumours such as osteosarcoma. Caffeine affects tumour cells through various pathways, including phosphatase and tensin homolog deleted on chromosome 10 (PTEN), AKT, Bcl-2-associated X protein (BAX), caspase-3 and p53, and has therefore been indicated as being useful for the treatment of malignant tumours. Here, the effects of caffeine on the proliferation of HOS osteosarcoma cells were assessed by WST-8 assay, and the effects on the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK) pathways were assessed by western blot analyses. Caffeine inhibited proliferation of HOS cells and suppressed NF-κB, AKT, mTOR/S6K and ERK activities. Our results support those from previous studies relating to the use of caffeine in the treatment of osteosarcoma.
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【Caffeine induces apoptosis of osteosarcoma cells by inhibiting AKT/mTOR/S6K, NF-κB and MAPK pathways.].
【咖啡因通过抑制AKT / mTOR / S6K，NF-κB和MAPK途径诱导骨肉瘤细胞凋亡。】
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DOI：文章类型：杂志文章
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：我们之前曾报道过咖啡因辅助的化疗改善了恶性骨和软组织肿瘤（如骨肉瘤）的治疗。咖啡因通过多种途径影响肿瘤细胞，包括在10号染色体（PTEN），AKT，Bcl-2相关X蛋白（BAX），caspase-3和p53缺失的磷酸酶和张力蛋白同源物，因此已被证明可用于恶性肿瘤的治疗。在这里，通过WST-8分析评估了咖啡因对HOS骨肉瘤细胞增殖的影响，以及对活化的B细胞（雷帕霉素的哺乳动物靶标）的核因子κ-轻链增强子（NF-κB）的影响（通过蛋白质印迹分析评估了mTOR）和有丝分裂原激活的蛋白激酶（MAPK）途径。咖啡因可抑制HOS细胞增殖，并抑制NF-κB，AKT，mTOR / S6K和ERK活性。我们的研究结果支持先前有关使用咖啡因治疗骨肉瘤的研究。
