背景:乳腺癌是最常见的恶性肿瘤,也是女性癌症相关死亡的主要原因。EC分泌的EGFR配体激活EGFR促进乳腺癌进展。目前的治疗在三阴性乳腺癌(TNBC)中提供有限的益处。光动力疗法(PDT)已被证明可通过EGFR途径治疗TNBC,但潜在的机制仍不清楚。
目的:本研究的目的是确定EGFR途径在共培养系统中对TNBC的PDT治疗中的作用。
方法:将MB-231和HUVEC共培养用于实验(HU-231)。AE-PDT后检测细胞活力和ROS产生,EGFR抑制剂(AEE788)与PDT的组合来测试血管生成,凋亡,和焦亡。WB检测EGFR的表达。EGFR,P-EGFR,VEGF,caspase-1、capase-3和GSDMD。
结果:AE-PDT抑制HU-231细胞增殖和肿瘤血管生成,并通过促进ROS产生诱导细胞凋亡和焦亡。AEE788,EGFR的抑制剂,AE-PDT后HU-231细胞杀伤增强。
结论:我们的研究表明,EGFR抑制剂和AE-PDT的组合可以协同抑制乳腺癌的进展,提供新的治疗策略。
Breast cancer is the most frequently diagnosed malignancy and the leading cause of cancerrelated deaths in women. Activation of EGFR by EC-secreted EGFR ligands promotes breast cancer progression. Current treatments provide limited benefits in triple-negative breast cancer (TNBC). Photodynamic therapy (PDT) has been proven effective for the treatment of TNBC through the EGFR pathway, but the underlying mechanism is still unclear.
The purpose of this study was to determine the role of the EGFR pathway in the treatment of PDT on TNBC in a co-culture system.
MB-231 and HUVEC were co-cultured for experiments (HU-231). Cell viability and ROS production were detected after AE-PDT, a combination of EGFR inhibitors (AEE788)with PDT to test angiogenesis, apoptosis, and pyroptosis. WB detects expression of EGFR. EGFR, P-EGFR, VEGF, caspase-1, capase-3, and GSDMD .
AE-PDT inhibited HU-231 cell proliferation and tumor angiogenesis, and induced cell apoptosis and pyroptosis by promoting ROS production. AEE788, an inhibitor of the EGFR, enhanced HU-231 cell killing after AE-PDT.
Our study suggested that the combination of EGFR inhibitors and AE-PDT could synergistically suppress breast cancer progression, providing a new treatment strategy.