Laboratory of Molecular Mechanisms of Carcinogenesis and Molecular Endocrinology, Instituto de Biología y Medicina Experimental (IBYME), CONICET, Vuelta de Obligado 2490, C1428ADN, Buenos Aires, Argentina.
Departamento de Anatomía Patológica (BIOREN), Universidad de La Frontera, Temuco, Chile.
Horm Cancer. 2020 Oct;11(5-6):218-239. doi: 10.1007/s12672-020-00392-4. Epub 2020 Jul 6.
The hormone receptor-positive (estrogen and/or progesterone receptor (PR)-positive) and HER2-negative breast cancer (BC) subtype is a biologically heterogeneous entity that includes luminal A-like (LumA-like) and luminal B-like (LumB-like) subtypes. Decreased PR levels is a distinctive biological feature of LumB-like tumors. These tumors also show reduced sensitivity to endocrine therapies and poorer prognosis than LumA-like tumors. Identification of biomarkers to accurately predict disease relapse in these subtypes is crucial in order to select effective therapies. We identified the tumor suppressor PDCD4 (programmed cell death 4), located in the nucleus (NPDCD4), as an independent prognostic factor of good clinical outcome in LumA-like and LumB-like subtypes. NPDCD4-positive LumB-like tumors presented overall and disease-free survival rates comparable to those of NPDCD4-positive LumA-like tumors, indicating that NPDCD4 improves the outcome of LumB-like patients. In contrast, NPDCD4 loss increased the risk of disease recurrence and death in LumB-like compared with LumA-like tumors. This, along with our results showing that LumB-like tumors present lower NPDCD4 positivity than LumA-like tumors, suggests that NPDCD4 loss contributes to endocrine therapy resistance in LumB-like BCs. We also revealed that PR induces PDCD4 transcription in LumB-like BC, providing a mechanistic explanation to the low PDCD4 levels in LumB-like BCs lacking PR. Finally, PDCD4 silencing enhanced BC cell survival in a patient-derived explant model of LumB-like disease. Our discoveries highlight NPDCD4 as a novel biomarker in LumA- and LumB-like subtypes, which could be included in the panel of immunohistochemical markers used in the clinic to accurately predict the prognosis of LumB-like tumors.
激素受体阳性(雌激素和/或孕激素受体(PR)阳性)和 HER2 阴性乳腺癌(BC)亚型是一种具有生物学异质性的实体,包括 luminal A 样(LumA-like)和 luminal B 样(LumB-like)亚型。PR 水平降低是 LumB-like 肿瘤的一个独特生物学特征。与 LumA-like 肿瘤相比,这些肿瘤对内分泌治疗的敏感性降低,预后较差。识别能够准确预测这些亚型疾病复发的生物标志物对于选择有效的治疗方法至关重要。我们发现位于细胞核内的肿瘤抑制因子 PDCD4(程序性细胞死亡因子 4)(NPDCD4)是 LumA-like 和 LumB-like 亚型的独立预后因素。NPDCD4 阳性的 LumB-like 肿瘤的总生存率和无病生存率与 NPDCD4 阳性的 LumA-like 肿瘤相当,表明 NPDCD4 改善了 LumB-like 患者的预后。相比之下,NPDCD4 的缺失增加了 LumB-like 肿瘤与 LumA-like 肿瘤相比疾病复发和死亡的风险。这与我们的结果表明 LumB-like 肿瘤的 NPDCD4 阳性率低于 LumA-like 肿瘤一致,表明 NPDCD4 缺失导致 LumB-like BC 对内分泌治疗的耐药性。我们还揭示了 PR 在 LumB-like BC 中诱导 PDCD4 转录,为 PR 缺失的 LumB-like BC 中 PDCD4 水平较低提供了一种机制解释。最后,PDCD4 沉默增强了 LumB-like 疾病患者衍生外植体模型中 BC 细胞的存活。我们的发现突出了 NPDCD4 作为 LumA-和 LumB-like 亚型的新型生物标志物,它可以包含在用于临床的免疫组织化学标志物面板中,以准确预测 LumB-like 肿瘤的预后。