目前的研究采用了 7,12-二甲基苯并(a)蒽 (DMBA) 诱导乳腺癌的动物模型。雌激素受体阳性人乳腺癌细胞系（MCF-7）用于体外分析。结合基于网络药理学的方法来评估螺旋藻 (SP) 提取物的抗癌特性并了解其分子机制。结果表明，施用1g/kg的SP通过提高过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的水平，同时降低丙二醛（MDA）和蛋白质羰基的水平来增加抗氧化活性。组织学检查显示，SP 保护的动物肿瘤发生率降低、雌激素受体表达降低、细胞增殖抑制、细胞凋亡促进。此外，SP 破坏了 MCF-7 细胞周期的 G2/M 期，诱导细胞凋亡和活性氧 (ROS) 积累。它还通过上调细胞色素 c、Bax、caspase-8、caspase-9 和 caspase-7 蛋白，同时下调 Bcl-2 的产生来增强 MCF-7 细胞的内在凋亡。 SP 的 LC-MS/MS 研究中鉴定出的主要化合物是肉桂酸、桧木素、戊酸和 α-亚麻酸的 7-羟基香豆素衍生物。这些物质专门针对三种重要的蛋白质：ERK1/2 MAPK、PI3K 蛋白激酶 B (AKT) 和表皮生长因子受体 (EGFR)。网络分析和分子对接表明 SP 和这些蛋白质之间存在显着的结合亲和力。蛋白质印迹分析证实了这一点，显示 SP 给药后 p-EGFR、p-ERK1/2 和 p-AKT 的蛋白水平降低。最后据报道，SP 通过调节 PI3K/AKT/EGFR 和 MAPK 信号通路来抑制 MCF-7 细胞生长并诱导细胞凋亡，表明 EGFR 作为 SP 在乳腺癌 (BC) 治疗中的潜在靶点。

The current research employed an animal model of 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary gland carcinogenesis. The estrogen receptor-positive human breast adenocarcinoma cell line (MCF-7) was used for in vitro analysis. This was combined with a network pharmacology-based approach to assess the anticancer properties of Spirulina (SP) extract and understand its molecular mechanisms. The results showed that the administration of 1 g/kg of SP increased the antioxidant activity by raising levels of catalase (CAT) and superoxide dismutase (SOD), while decreasing the levels of malonaldehyde (MDA) and protein carbonyl. A histological examination revealed reduced tumor occurrence, decreased estrogen receptor expression, suppressed cell proliferation, and promoted apoptosis in SP protected animals. In addition, SP disrupted the G2/M phase of the MCF-7 cell cycle, inducing apoptosis and reactive oxygen species (ROS) accumulation. It also enhanced intrinsic apoptosis in MCF-7 cells by upregulating cytochrome c, Bax, caspase-8, caspase-9, and caspase-7 proteins, while downregulating Bcl-2 production. The main compounds identified in the LC-MS/MS study of SP were 7-hydroxycoumarin derivatives of cinnamic acid, hinokinin, valeric acid, and α-linolenic acid. These substances specifically targeted three important proteins: ERK1/2 MAPK, PI3K-protein kinase B (AKT), and the epidermal growth factor receptor (EGFR). Network analysis and molecular docking indicated a significant binding affinity between SP and these proteins. This was verified by Western blot analysis that revealed decreased protein levels of p-EGFR, p-ERK1/2, and p-AKT following SP administration. SP was finally reported to suppress MCF-7 cell growth and induce apoptosis by modulating the PI3K/AKT/EGFR and MAPK signaling pathways suggesting EGFR as a potential target of SP in breast cancer (BC) treatment.