Manas Sehgal, Sonali Priyadarshini Nayak, Sarthak Sahoo, Jason A Somarelli, Mohit Kumar Jolly
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引用次数: 0
摘要
神经母细胞瘤是最常见的颅外儿科肿瘤,导致15%的儿童死于癌症。神经母细胞瘤的肿瘤复发和耐药性是由去甲肾上腺素能(NOR)细胞和间质(MES)细胞状态之间的表型可塑性和异质性驱动的。尽管这种表型可塑性非常重要,但与这些双向细胞状态转换相关的动力学和分子模式仍然知之甚少。在这里,我们分析了大体和单细胞分辨率的多个 RNA-seq 数据集,以了解 NOR 和 MES 特异性因子之间的关联。我们观察到,NOR 特异性和 MES 特异性表达模式在很大程度上是相互排斥的,在相关基因中表现出一种 "团队 "行为,这让人想起我们早先在肺癌和黑色素瘤中观察到的现象。NOR 和 MES 表型之间的这种拮抗作用还与代谢重编程、免疫疗法靶标 PD-L1 和 GD2 以及驱动 NOR-MES 和/或 MES-NOR 转化的实验扰动有关。此外,这些 "类似团队 "的模式只出现在NOR和MES特异性基因中,而不出现在保守基因中,这可能凸显了使癌细胞具有可塑性的网络拓扑特征。
Mutually exclusive teams-like patterns of gene regulation characterize phenotypic heterogeneity along the noradrenergic-mesenchymal axis in neuroblastoma.
Neuroblastoma is the most frequent extracranial pediatric tumor and leads to 15% of all cancer-related deaths in children. Tumor relapse and therapy resistance in neuroblastoma are driven by phenotypic plasticity and heterogeneity between noradrenergic (NOR) and mesenchymal (MES) cell states. Despite the importance of this phenotypic plasticity, the dynamics and molecular patterns associated with these bidirectional cell-state transitions remain relatively poorly understood. Here, we analyze multiple RNA-seq datasets at both bulk and single-cell resolution, to understand the association between NOR- and MES-specific factors. We observed that NOR-specific and MES-specific expression patterns are largely mutually exclusive, exhibiting a "teams-like" behavior among the genes involved, reminiscent of our earlier observations in lung cancer and melanoma. This antagonism between NOR and MES phenotypes was also associated with metabolic reprogramming and with immunotherapy targets PD-L1 and GD2 as well as with experimental perturbations driving the NOR-MES and/or MES-NOR transition. Further, these "teams-like" patterns were seen only among the NOR- and MES-specific genes, but not in housekeeping genes, possibly highlighting a hallmark of network topology enabling cancer cell plasticity.
期刊介绍:
Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.