雄激素受体 (AR) 已作为一种癌症治疗方法进行了研究。除了前列腺癌衍生的 LNCaP 和 DU-145 细胞外，我们还使用了 AR 高、低和极低表达水平的人乳腺癌衍生细胞作为阳性和阴性对照，检查由针对 AR 的合成肽引起的细胞凋亡。该肽的产生是为了抑制乳腺癌细胞系中的 AR 反式激活。然后我们测量了细胞活力、caspase-3 活性和 Bax/Bcl-2 的比率。研究结果表明，在存在二氢睾酮 (DHT) 的情况下，肽 (100-500nM) 会降低 AR 表达水平高和低的细胞的细胞生长 (p < .001)，但 AR 水平非常低的细胞不会减少细胞生长。用 100-500nM 肽处理可激活 caspase-3，并增加 AR 高表达和低表达水平细胞中 Bax/Bcl-2 的比率。此外，在存在 DHT 的情况下，增加肽的浓度 (100-500nM) 会减少 BrdU 的掺入，并促进 AR 高表达和低表达水平的细胞凋亡 (p< .001)。研究结果表明，肽显着增加了细胞凋亡癌细胞。© 2023 作者。由 Wiley periodicals LLC 出版的癌症报告。

The androgen receptor (AR) has been studied as an approach to cancer therapy.We used human breast cancer-derived cells with high, low, and very low expression levels of AR, in addition to prostate cancer-derived LNCaP and DU-145 cells as a positive and negative controls to examine apoptosis caused by a synthetic peptide that targets ARs.The peptide was produced to inhibit AR transactivation in breast cancer cell lines. We then measured cell viability, caspase-3 activity, and the ratio of Bax/Bcl-2. The findings indicated that the peptide (100-500 nM) in the presence of dihydrotestosterone (DHT) reduced cell growth in cells with high and low expression level of AR (p < .001), but not in cells with very low levels of AR. Treatment with 100-500 nM of peptide activated caspase-3 and increased the ratio of Bax/Bcl-2 in cells with high and low expression levels of AR. Also, increasing concentrations of the peptide (100-500 nM) reduced BrdU incorporation in the presence of DHT and promoted apoptosis in cells with high and low expression levels of AR (p < .001).The findings indicate the peptide significantly increased apoptosis in cancer cells.© 2023 The Authors. Cancer Reports published by Wiley Periodicals LLC.