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BCL9 provides multi-cellular communication properties in colorectal cancer by interacting with paraspeckle proteins.
Nature Communications ( IF 14.7 ) Pub Date : 2020-01-07 , DOI: 10.1038/s41467-019-13842-7 Meng Jiang 1, 2 , Yue Kang 1, 3 , Tomasz Sewastianik 1, 4 , Jiao Wang 1, 5 , Helen Tanton 1 , Keith Alder 1 , Peter Dennis 1 , Yu Xin 1 , Zhongqiu Wang 1, 6 , Ruiyang Liu 1 , Mengyun Zhang 1 , Ying Huang 1 , Massimo Loda 1 , Amitabh Srivastava 7 , Runsheng Chen 3 , Ming Liu 2 , Ruben D Carrasco 1, 7
Nature Communications ( IF 14.7 ) Pub Date : 2020-01-07 , DOI: 10.1038/s41467-019-13842-7 Meng Jiang 1, 2 , Yue Kang 1, 3 , Tomasz Sewastianik 1, 4 , Jiao Wang 1, 5 , Helen Tanton 1 , Keith Alder 1 , Peter Dennis 1 , Yu Xin 1 , Zhongqiu Wang 1, 6 , Ruiyang Liu 1 , Mengyun Zhang 1 , Ying Huang 1 , Massimo Loda 1 , Amitabh Srivastava 7 , Runsheng Chen 3 , Ming Liu 2 , Ruben D Carrasco 1, 7
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Colorectal cancer (CRC) is the third most commonly diagnosed cancer, which despite recent advances in treatment, remains incurable due to molecular heterogeneity of tumor cells. The B-cell lymphoma 9 (BCL9) oncogene functions as a transcriptional co-activator of the Wnt/β-catenin pathway, which plays critical roles in CRC pathogenesis. Here we have identified a β-catenin-independent function of BCL9 in a poor-prognosis subtype of CRC tumors characterized by expression of stromal and neural associated genes. In response to spontaneous calcium transients or cellular stress, BCL9 is recruited adjacent to the interchromosomal regions, where it stabilizes the mRNA of calcium signaling and neural associated genes by interacting with paraspeckle proteins. BCL9 subsequently promotes tumor progression and remodeling of the tumor microenvironment (TME) by sustaining the calcium transients and neurotransmitter-dependent communication among CRC cells. These data provide additional insights into the role of BCL9 in tumor pathogenesis and point towards additional avenues for therapeutic intervention.
中文翻译：
BCL9通过与散斑蛋白相互作用，在结直肠癌中提供了多细胞通讯特性。
大肠癌（CRC）是第三大最常被诊断的癌症，尽管最近在治疗方面取得了进步，但由于肿瘤细胞的分子异质性，其仍无法治愈。B细胞淋巴瘤9（BCL9）癌基因充当Wnt /β-catenin途径的转录共激活因子，在CRC发病机理中起关键作用。在这里，我们已经确定了以基质和神经相关基因表达为特征的预后不良的CRC肿瘤中BCL9的β-catenin依赖性功能。响应自发的钙瞬变或细胞应激，BCL9被募集到染色体间区域附近，在那里它通过与副斑点蛋白相互作用来稳定钙信号和神经相关基因的mRNA。BCL9随后通过维持CRC细胞之间的钙瞬变和神经递质依赖性通讯来促进肿瘤进展和肿瘤微环境（TME）重塑。这些数据提供了有关BCL9在肿瘤发病机制中作用的更多见解，并为治疗干预指明了其他途径。
更新日期：2020-01-07
中文翻译：
BCL9通过与散斑蛋白相互作用，在结直肠癌中提供了多细胞通讯特性。
大肠癌（CRC）是第三大最常被诊断的癌症，尽管最近在治疗方面取得了进步，但由于肿瘤细胞的分子异质性，其仍无法治愈。B细胞淋巴瘤9（BCL9）癌基因充当Wnt /β-catenin途径的转录共激活因子，在CRC发病机理中起关键作用。在这里，我们已经确定了以基质和神经相关基因表达为特征的预后不良的CRC肿瘤中BCL9的β-catenin依赖性功能。响应自发的钙瞬变或细胞应激，BCL9被募集到染色体间区域附近，在那里它通过与副斑点蛋白相互作用来稳定钙信号和神经相关基因的mRNA。BCL9随后通过维持CRC细胞之间的钙瞬变和神经递质依赖性通讯来促进肿瘤进展和肿瘤微环境（TME）重塑。这些数据提供了有关BCL9在肿瘤发病机制中作用的更多见解，并为治疗干预指明了其他途径。
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