Background: Breast cancer (BC) is the most common cancer in women worldwide. Much progress has been made to improve treatment options for patients suffering from the disease, including a novel therapy—Poly (ADP-ribose) polymerase inhibitor (PARPi) that specifically targets tumors with deficiencies in the Homologous Recombination (HR) DNA repair pathway. To benefit better from conventional therapy, many patients seek alternative supplementation, with 20–30% of cancer patients using herbal medication on top of their regular treatment. An example of such easily available over-the-counter supplements is curcumin, a natural compound derived from turmeric (Curcuma longa). Various studies reported the potential HR deficiency (HRD) inducing effect of curcumin in cancer cells.Methods: Eight BrC and three normal cell lines and a BrC PDX model were used to evaluate the effect of curcumin on RAD51 ionizing radiation-induced focus (IRIF) formation. Three breast BrC cell lines underwent further analysis using the BRCA2 Western blot technique. To assess cell survival after treatment with curcumin and/or PARPi, a clonogenic survival assay was performed on both normal and cancerous cell lines.Results: Curcumin treatment led to a reduction in RAD51 IRIF formation capacity across all tested models. A decrease in BRCA2 levels was observed in the tested cell lines. Our findings demonstrate that HRD can be induced in both cancerous and normal cells, suggesting that curcumin treatment may increase the risk of toxicity when combined with PARPi therapy.Conclusions: The use of curcumin in combination with certain anti-cancer treatments should not be implemented without extensive monitoring for deleterious side effects.
背景：乳腺癌是全球女性最常见的恶性肿瘤。针对该疾病的治疗方案已取得显著进展，其中新型疗法——聚腺苷二磷酸核糖聚合酶抑制剂通过特异性靶向同源重组DNA修复通路缺陷的肿瘤发挥作用。为提升传统治疗获益，约20-30%的癌症患者在常规治疗基础上寻求草本药物补充。姜黄素作为从姜黄中提取的天然化合物，是此类非处方补充剂的典型代表。多项研究报道姜黄素可能诱导癌细胞产生同源重组缺陷。 方法：本研究采用八种乳腺癌细胞系、三种正常细胞系及乳腺癌患者来源异种移植模型，评估姜黄素对RAD51电离辐射诱导灶形成的影响。通过BRCA2蛋白印迹技术对三种乳腺癌细胞系进行深入分析。采用克隆形成实验检测正常与癌细胞系在姜黄素和/或PARPi处理后的细胞存活情况。 结果：姜黄素处理导致所有测试模型中RAD51电离辐射诱导灶形成能力下降。受试细胞系中观察到BRCA2蛋白水平降低。研究证实姜黄素能在癌细胞和正常细胞中诱导同源重组缺陷，提示其与PARPi联合治疗可能增加毒性风险。 结论：姜黄素与特定抗癌疗法联用时，需在严格监测有害副作用的前提下谨慎使用。
肿瘤(癌症)患者之家