Department of Urology, The Gongli Hospital of Second Military Medical University.
Department of Urology, The Third Affiliated Hospital of Second Military Medical University (Eastern Hepatobiliary Surgery Hospital), Shanghai.
Anticancer Drugs. 2018 Oct;29(9):839-846. doi: 10.1097/CAD.0000000000000666.
Testicular cancer (TC) is the most common malignancy in men. Although the 5-year survival rate of TC patients exceeds 95%, the prognosis of patients with platinum-resistant tumors remains poor because of limited therapeutic options. Overcoming chemoresistance is the key to improving survival in poor-prognosis patients. However, the mechanism remains poorly understood. B-cell lymphoma 2 ovarian killer (BOK) is a proapoptotic protein and functions as a tumor suppressor in malignancy tumors. In this study, we found that BOK was frequently downregulated in TC tissues compared with paratumor tissues. BOK overexpression inhibited TC cell proliferation and invasion. In contrast, BOK knockdown promoted TC cell proliferation and invasion. Surprisingly, either BOK overexpression or knockdown rendered TC cells resistant to Cisplatin (DDP). In conclusion, BOK downregulation may be associated with tumorigenesis of TC. BOK had the potency to suppress TC cell proliferation and invasion, and may function as a tumor suppressor in TC. However, BOK also contributes to Cisplatin resistance. These data may provide a wider perspective on TC research and treatment.
睾丸癌（TC）是男性中最常见的恶性肿瘤。尽管 TC 患者的 5 年生存率超过 95%，但由于治疗选择有限，铂耐药肿瘤患者的预后仍然较差。克服化疗耐药性是改善预后不良患者生存的关键。然而，其机制仍知之甚少。B 细胞淋巴瘤 2 卵巢杀手（BOK）是一种促凋亡蛋白，在恶性肿瘤中作为肿瘤抑制因子发挥作用。在这项研究中，我们发现与肿瘤旁组织相比，BOK 在 TC 组织中经常下调。BOK 过表达抑制 TC 细胞增殖和侵袭。相比之下，BOK 敲低促进 TC 细胞增殖和侵袭。令人惊讶的是，BOK 的过表达或敲低使 TC 细胞对顺铂（DDP）产生耐药性。总之，BOK 的下调可能与 TC 的发生有关。BOK 具有抑制 TC 细胞增殖和侵袭的能力，可能在 TC 中作为肿瘤抑制因子发挥作用。然而，BOK 也有助于顺铂耐药性。这些数据可能为 TC 的研究和治疗提供更广泛的视角。
