Department of Oncology, Barbara Ann Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI, USA.
Department of Computer Science, Wayne State University, Detroit, MI, USA.
Mol Oncol. 2019 Apr;13(4):894-908. doi: 10.1002/1878-0261.12444. Epub 2019 Mar 1.
Obesity is a risk factor for triple-negative breast cancer (TNBC) incidence and poor outcomes, but the underlying molecular biology remains unknown. We previously identified in TNBC cell cultures that expression of epigenetic reader methyl-CpG-binding domain protein 2 (MBD2), specifically the alternative mRNA splicing variant MBD variant 2 (MBD2_v2), is dependent on reactive oxygen species (ROS) and is crucial for maintenance and expansion of cancer stem cell-like cells (CSCs). Because obesity is coupled with inflammation and ROS, we hypothesized that obesity can fuel an increase in MBD2_v2 expression to promote the tumor-initiating CSC phenotype in TNBC cells in vivo. Analysis of TNBC patient datasets revealed associations between high tumor MBD2_v2 expression and high relapse rates and high body mass index (BMI). Stable gene knockdown/overexpression methods were applied to TNBC cell lines to elucidate that MBD2_v2 expression is governed by ROS-dependent expression of serine- and arginine-rich splicing factor 2 (SRSF2). We employed a diet-induced obesity (DIO) mouse model that mimics human obesity to investigate whether obesity causes increased MBD2_v2 expression and increased tumor initiation capacity in inoculated TNBC cell lines. MBD2_v2 and SRSF2 levels were increased in TNBC cell line-derived tumors that formed more frequently in DIO mice relative to tumors in lean control mice. Stable MBD2_v2 overexpression increased the CSC fraction in culture and increased TNBC cell line tumor initiation capacity in vivo. SRSF2 knockdown resulted in decreased MBD2_v2 expression, decreased CSCs in TNBC cell cultures, and hindered tumor formation in vivo. This report describes evidence to support the conclusion that MBD2_v2 expression is induced by obesity and drives TNBC cell tumorigenicity, and thus provides molecular insights into support of the epidemiological evidence that obesity is a risk factor for TNBC. The majority of TNBC patients are obese and rising obesity rates threaten to further increase the burden of obesity-linked cancers, which reinforces the relevance of this report.
肥胖是三阴性乳腺癌 (TNBC) 发病和预后不良的一个风险因素,但潜在的分子生物学机制尚不清楚。我们之前在 TNBC 细胞培养中发现,表观遗传阅读器甲基-CpG 结合域蛋白 2 (MBD2) 的表达,特别是选择性剪接变体 MBD 变体 2 (MBD2_v2) 的表达,依赖于活性氧 (ROS),对于维持和扩增癌症干细胞样细胞 (CSCs) 至关重要。由于肥胖与炎症和 ROS 有关,我们假设肥胖可以增加 MBD2_v2 的表达,从而促进 TNBC 细胞中肿瘤起始 CSC 表型的形成。对 TNBC 患者数据集的分析显示,高肿瘤 MBD2_v2 表达与高复发率和高体重指数 (BMI) 之间存在关联。TNBC 细胞系中应用稳定的基因敲低/过表达方法表明,MBD2_v2 的表达受 ROS 依赖性丝氨酸/精氨酸丰富剪接因子 2 (SRSF2) 的表达调控。我们采用饮食诱导肥胖 (DIO) 小鼠模型来模拟人类肥胖,以研究肥胖是否会导致接种的 TNBC 细胞系中 MBD2_v2 表达增加和肿瘤起始能力增强。与瘦对照小鼠相比,DIO 小鼠中形成的 TNBC 细胞系衍生肿瘤中 MBD2_v2 和 SRSF2 水平升高。稳定过表达 MBD2_v2 增加了培养物中的 CSC 分数,并增加了 TNBC 细胞系在体内的肿瘤起始能力。SRSF2 敲低导致 MBD2_v2 表达降低,TNBC 细胞培养中的 CSCs 减少,体内肿瘤形成受阻。本报告提供了证据支持以下结论:MBD2_v2 的表达是由肥胖诱导的,并驱动 TNBC 细胞的致瘤性,从而为肥胖是 TNBC 风险因素的流行病学证据提供了分子依据。大多数 TNBC 患者肥胖,肥胖率上升有可能进一步增加肥胖相关癌症的负担,这进一步强调了本报告的相关性。