Department of Medical Biology, Faculty of Medicine, Biruni University, Istanbul, Turkey.
Department of Biochemistry, Faculty of Pharmacy, Istanbul Health and Technology University, Istanbul, Turkey.
Photodiagnosis Photodyn Ther. 2023 Dec;44:103849. doi: 10.1016/j.pdpdt.2023.103849. Epub 2023 Oct 18.
Breast cancer is the most common cancer affecting women worldwide.Photodynamic therapy(PDT) has now proven to be a promising form of cancer therapy due to its targeted and low cytotoxicity to healthy cells and tissues.PDT is a technique used to create cell death localized by light after application of a light-sensitive agent.Aza-BODIPY is a promising photosensitizer for use in PDT. Our results showed that aza-BODIPY-PDT induced apoptosis, probably through p53 and caspase3 in MCF-7 cells. Future studies should delineate the molecular mechanisms underlying aza-BODIPY-PDT-induced cell death for a better understanding of the signaling pathways modulated by the therapy so that this novel technology could be implemented in the clinic for treating breast cancer.
In this study,we aimed to determine the change in the expression levels of 88 carcinoma-associated genes induced by aza-BODIPY-PDT were analyzed so as to understand the specific pathways that are modulated by aza-BODIPY-PDT.
In this study,the molecular basis of the anti-cancer activity of aza-BODIPY-PDT was investigated.Induction of apoptosis and necrosis in MCF-7 breast cancer cells after treatment with aza- BODIPY derivative with phthalonitrile substituents (aza-BODIPY) followed by light exposure was evaluated by Annexin V 7- Aminoactinomycin D (7-AAD) flow cytometry.
Aza-BODIPY-PDT induced cell death in MCF-7 cells treated with aza-BODIPY-PDT; flow cytometry revealed that 28 % of the cells died by apoptosis. Seven of the 88 carcinoma-associated genes that were assayed were differentially expressed -EGF, LEF1, WNT1, TCF7, and TGFBR2 were downregulated, and CASP3 and TP53 were upregulated - in cells subjected to aza-BODIPY-PDT.This made us think that the aza-BODIPY-PDT induced caspase 3 and p53-mediated apoptosis in MCF7 cells.
In our study,it was determined that the application of aza-BODIPY-PDT to MCF7 cells had a negative effect on cell connectivity and cell cycle.The fact that the same effect was not observed in control cells and MCF7 cells in the dark field of aza-BODIPY indicates that aza-BODIPY has a strong phodynamic anticancer effect.
乳腺癌是全球女性最常见的癌症。光动力疗法（PDT）由于对健康细胞和组织的靶向性和低细胞毒性，现已被证明是一种很有前途的癌症治疗形式。PDT 是一种在应用光敏剂后通过光将细胞死亡局限化的技术。Aza-BODIPY 是一种很有前途的用于 PDT 的光敏剂。我们的结果表明，aza-BODIPY-PDT 诱导 MCF-7 细胞凋亡，可能通过 p53 和 caspase3。未来的研究应该阐明 aza-BODIPY-PDT 诱导细胞死亡的分子机制，以便更好地理解该疗法调节的信号通路，从而将这项新技术应用于临床治疗乳腺癌。
在这项研究中，我们旨在确定 aza-BODIPY-PDT 诱导的 88 种癌相关基因表达水平的变化，以了解 aza-BODIPY-PDT 调节的特定途径。
在这项研究中，研究了 aza-BODIPY-PDT 的抗癌活性的分子基础。用带有苯并二氮杂菲取代基的 aza-BODIPY 衍生物（aza-BODIPY）处理 MCF-7 乳腺癌细胞后，通过 Annexin V 7-氨基放线菌素 D（7-AAD）流式细胞术评估细胞凋亡和坏死的诱导。
用 aza-BODIPY-PDT 处理的 MCF-7 细胞中，aza-BODIPY-PDT 诱导细胞死亡；流式细胞术显示 28%的细胞通过凋亡死亡。在接受 aza-BODIPY-PDT 的细胞中，88 种癌相关基因中有 7 种表达差异——EGF、LEF1、WNT1、TCF7 和 TGFBR2 下调，CASP3 和 TP53 上调——这使我们认为 aza-BODIPY-PDT 诱导 MCF7 细胞中 caspase 3 和 p53 介导的凋亡。
在我们的研究中，确定了 aza-BODIPY-PDT 应用于 MCF7 细胞对细胞连接和细胞周期有负面影响。在黑暗场中观察到 aza-BODIPY 对 MCF7 细胞没有相同的影响，这表明 aza-BODIPY 具有很强的光动力抗癌作用。
