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首页> 外文期刊>Cell cycle >Nodal expression in triple-negative breast cancer: Cellular effects of its inhibition following doxorubicin treatment
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Nodal expression in triple-negative breast cancer: Cellular effects of its inhibition following doxorubicin treatment

机译：三阴性乳腺癌中的淋巴结表达：阿霉素治疗后其抑制作用的细胞作用

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Triple-negative breast cancer (TNBC) represents an aggressive cancer subtype characterized by the lack of expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). The independence of TNBC from these growth promoting factors eliminates the efficacy of therapies which specifically target them, and limits TNBC patients to traditional systemic neo/adjuvant chemotherapy. To better understand the growth advantage of TNBC - in the absence of ER, PR and HER2, we focused on the embryonic morphogen Nodal (associated with the cancer stem cell phenotype), which is re-expressed in aggressive breast cancers. Most notably, our previous data demonstrated that inhibition of Nodal signaling in breast cancer cells reduces their tumorigenic capacity. Furthermore, inhibiting Nodal in other cancers has resulted in improved effects of chemotherapy, although the mechanisms for this remain unknown. Thus, we hypothesized that targeting Nodal in TNBC cells in combination with conventional chemotherapy may improve efficacy and represent a potential new strategy. Our preliminary data demonstrate that Nodal is highly expressed in TNBC when compared to invasive hormone receptor positive samples. Treatment of Nodal expressing TNBC cell lines with a neutralizing anti-Nodal antibody reduces the viability of cells that had previously survived treatment with the anthracycline doxorubicin. We show that inhibiting Nodal may alter response mechanisms employed by cancer cells undergoing DNA damage. These data suggest that development of therapies which target Nodal in TNBC may lead to additional treatment options in conjunction with chemotherapy regimens - by altering signaling pathways critical to cellular survival.
机译：三阴性乳腺癌（TNBC）代表一种侵略性癌症亚型，其特征是缺乏雌激素受体（ER），孕激素受体（PR）和人表皮生长因子受体2（HER2）的表达。 TNBC与这些生长促进因子的独立性消除了针对其的疗法的功效，并使TNBC患者只能使用传统的全身性新/辅助化疗。为了更好地了解TNBC的生长优势-在没有ER，PR和HER2的情况下，我们集中研究了胚胎形态发生子Nodal（与癌症干细胞表型有关），该基因在侵袭性乳腺癌中重新表达。最值得注意的是，我们之前的数据表明，抑制乳腺癌细胞中的Nodal信号传导会降低其致瘤能力。此外，在其他癌症中抑制Nodal可以提高化疗效果，尽管其机制尚不清楚。因此，我们假设与常规化学疗法联合在TNBC细胞中靶向Nodal可以提高疗效，并代表了一种潜在的新策略。我们的初步数据表明，与浸润性激素受体阳性样品相比，Nodal在TNBC中高表达。用中和性抗Nodal抗体处理表达Nodal的TNBC细胞系会降低以前用蒽环霉素阿霉素处理后仍然存活的细胞的活力。我们表明抑制Nodal可能会改变癌细胞遭受DNA损伤的反应机制。这些数据表明针对TNBC中Nodal的疗法的发展可能通过改变对细胞存活至关重要的信号传导途径，与化学疗法相结合，可能导致更多的治疗选择。

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