Department of Nuclear Medicine, Tianjin Medical University General Hospital, Anshan Road No. 154, He ping District, Tianjin, 300052, P.R. China.
Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Tianjin Medical University, Tianjin, 300070, P. R. China.
BMC Cancer. 2024 Jul 8;24(1):816. doi: 10.1186/s12885-024-12511-3.
Anaplastic thyroid carcinoma (ATC) is a rare but highly aggressive thyroid cancer with poor prognosis. Killing cancer cells by inducing DNA damage or blockage of DNA repair is a promising strategy for chemotherapy. It is reported that aldehyde-reactive alkoxyamines can capture the AP sites, one of the most common DNA lesions, and inhibit apurinic/apyrimidinic endonuclease 1(APE1)-mediated base excision repair (BER), leading to cell death. Whether this strategy can be employed for ATC treatment is rarely investigated. The aim of this study is to exploit GSH-responsive AP site capture reagent (AP probe-net), which responses to the elevated glutathione (GSH) levels in the tumor micro-environment (TME), releasing reactive alkoxyamine to trap AP sites and block the APE1-mediated BER for targeted anti-tumor activity against ATC. In vitro experiments, including MTT andγ-H2AX assays, demonstrate their selective cytotoxicity towards ATC cells over normal thyroid cells. Flow cytometry analysis suggests that AP probe-net arrests the cell cycle in the G2/M phase and induces apoptosis. Western blotting (WB) results show that the expression of apoptotic protein increased with the increased concentration of AP probe-net. Further in vivo experiments reveal that the AP probe-net has a good therapeutic effect on subcutaneous tumors of the ATC cells. In conclusion, taking advantage of the elevated GSH in TME, our study affords a new strategy for targeted chemotherapy of ATC with high selectivity and reduced adverse effects.
间变性甲状腺癌(ATC)是一种罕见但高度侵袭性的甲状腺癌,预后不良。通过诱导 DNA 损伤或阻断 DNA 修复来杀死癌细胞是化疗的一种有前途的策略。据报道,醛反应性烷氧基胺可以捕获 AP 位点,这是最常见的 DNA 损伤之一,并抑制脱嘌呤/脱嘧啶内切酶 1(APE1)介导的碱基切除修复(BER),导致细胞死亡。这种策略是否可用于 ATC 治疗很少被研究。本研究旨在利用 GSH 响应的 AP 位点捕获试剂(AP 探针网),该试剂响应肿瘤微环境(TME)中升高的谷胱甘肽(GSH)水平,释放反应性烷氧基胺以捕获 AP 位点并阻断 APE1 介导的 BER,从而针对 ATC 发挥靶向抗肿瘤活性。体外实验,包括 MTT 和γ-H2AX 测定,证明它们对 ATC 细胞具有选择性细胞毒性,而对正常甲状腺细胞没有毒性。流式细胞术分析表明,AP 探针网将细胞周期阻滞在 G2/M 期并诱导细胞凋亡。Western blot(WB)结果表明,随着 AP 探针网浓度的增加,凋亡蛋白的表达增加。进一步的体内实验表明,AP 探针网对 ATC 细胞的皮下肿瘤具有良好的治疗效果。总之,利用 TME 中升高的 GSH,我们的研究为 ATC 的靶向化疗提供了一种新策略,具有高选择性和减少不良反应。