Carson Meredith S, Rädler Patrick D, Albright Jody, VerHague Melissa, Rezeli Erika T, Roth Daniel, French John E, Perou Charles M, Hursting Stephen D, Coleman Michael F
Department of Nutrition, University of North Carolina, Chapel Hill, NC 27599, USA.
Department of Genetics, University of North Carolina, Chapel Hill, NC 27599, USA.
Cancers (Basel). 2024 Aug 9;16(16):2803. doi: 10.3390/cancers16162803.
Obesity is an established risk and progression factor for triple-negative breast cancer (TNBC), but preclinical studies to delineate the mechanisms underlying the obesity-TNBC link as well as strategies to break that link are constrained by the lack of tumor models syngeneic to obesity-prone mouse strains. C3(1)/SV40 T-antigen (C3-TAg) transgenic mice on an FVB genetic background develop tumors with molecular and pathologic features that closely resemble human TNBC, but FVB mice are resistant to diet-induced obesity (DIO). Herein, we sought to develop transplantable C3-TAg cell lines syngeneic to C57BL/6 mice, an inbred mouse strain that is sensitive to DIO. We backcrossed FVB-Tg(C3-1-TAg)cJeg/JegJ to C57BL/6 mice for ten generations, and spontaneous tumors from those mice were excised and used to generate four clonal cell lines (B6TAg1.02, B6TAg2.03, B6TAg2.10, and B6TAg2.51). We characterized the growth of the four cell lines in both lean and DIO C57BL/6J female mice and performed transcriptomic profiling. Each cell line was readily tumorigenic and had transcriptional profiles that clustered as claudin-low, yet markedly differed from each other in their rate of tumor progression and transcriptomic signatures for key metabolic, immune, and oncogenic signaling pathways. DIO accelerated tumor growth of orthotopically transplanted B6TAg1.02, B6TAg2.03, and B6TAg2.51 cells. Thus, the B6TAg cell lines described herein offer promising and diverse new models to augment the study of DIO-associated TNBC.
肥胖是三阴性乳腺癌(TNBC)公认的风险和进展因素,但由于缺乏与易肥胖小鼠品系同源的肿瘤模型,用于阐明肥胖与TNBC之间联系的潜在机制以及打破这种联系的策略的临床前研究受到限制。FVB遗传背景的C3(1)/SV40 T抗原(C3-TAg)转基因小鼠所患肿瘤的分子和病理特征与人类TNBC极为相似,但FVB小鼠对饮食诱导的肥胖(DIO)具有抗性。在此,我们试图开发与C57BL/6小鼠同源的可移植C3-TAg细胞系,C57BL/6是一种对DIO敏感的近交小鼠品系。我们将FVB-Tg(C3-1-TAg)cJeg/JegJ与C57BL/6小鼠回交了十代,切除这些小鼠的自发肿瘤并用于生成四个克隆细胞系(B6TAg1.02、B6TAg2.03、B6TAg2.10和B6TAg2.51)。我们对这四个细胞系在瘦型和DIO C57BL/6J雌性小鼠中的生长情况进行了表征,并进行了转录组分析。每个细胞系都易于致瘤,其转录谱聚类为claudin-low,但它们在肿瘤进展速度以及关键代谢、免疫和致癌信号通路的转录组特征方面彼此明显不同。DIO加速了原位移植的B6TAg1.02、B6TAg2.03和B6TAg2.51细胞的肿瘤生长。因此,本文所述的B6TAg细胞系为加强对DIO相关TNBC的研究提供了有前景且多样的新模型。