Laboratory of Molecular Pathology, State University of Londrina, Londrina, PR, Brazil.
Laboratory of Pathophysiology and Muscle Adaptation, State University of Londrina, Londrina, PR, Brazil.
Nutr Cancer. 2021;73(8):1378-1388. doi: 10.1080/01635581.2020.1795693. Epub 2020 Jul 21.
To investigate the effects of caffeine on the proliferation and death of human breast cancer cells MCF-7 and MDA-MB-231. Cells were exposed to 1, 2.5, 5 and 10 mM of caffeine during 24 h, and oxidative stress (OS), cell proliferation and death, metabolic activity and DNA lesions were evaluated in the collected samples. Caffeine was cytotoxic to the cell lines analyzed, reducing cell proliferation and viability by interfering with the cellular metabolism and with lysosomal function. Although the cells presented different behaviors to treatment, in both cell lines, the drug induced OS and predominantly apoptosis. MCF-7 cells responded to OS induction (lipid peroxidation) increasing their antioxidant defenses. However, the OS generated induced oxidative DNA lesions, a finding not observed in MDA-MB-231 cells. The association of different scavengers with caffeine did not result in the recovery of cell viability, which suggests that it is not possible to attribute the caffeine induction of OS to only one of the specific ROS analyzed (superoxide anion, singlet oxygen and peroxyl radical). These results are promising and suggest that caffeine may be a good target for studies to prove its usefulness as an adjuvant in breast cancer treatment.
为了研究咖啡因对人乳腺癌 MCF-7 和 MDA-MB-231 细胞增殖和死亡的影响。将细胞暴露于 1、2.5、5 和 10 mM 的咖啡因中 24 小时，并在收集的样品中评估氧化应激（OS）、细胞增殖和死亡、代谢活性和 DNA 损伤。咖啡因对所分析的细胞系具有细胞毒性，通过干扰细胞代谢和溶酶体功能来降低细胞增殖和活力。尽管两种细胞系的细胞表现出不同的处理行为，但药物均诱导 OS 并主要诱导细胞凋亡。MCF-7 细胞对 OS 诱导（脂质过氧化）做出反应，增加其抗氧化防御能力。然而，在 MDA-MB-231 细胞中未观察到 OS 诱导的氧化 DNA 损伤。用不同的清除剂与咖啡因联合使用并没有恢复细胞活力，这表明咖啡因诱导的 OS 不能归因于分析的特定 ROS（超氧阴离子、单线态氧和过氧自由基）之一。这些结果很有希望，表明咖啡因可能是研究的一个很好的靶点，以证明其作为乳腺癌治疗辅助剂的有用性。
