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首页> 外文期刊>Journal of Cellular Physiology >RB1 in cancer: Different mechanisms of RB1 inactivation and alterations of pRb pathway in tumorigenesis
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RB1 in cancer: Different mechanisms of RB1 inactivation and alterations of pRb pathway in tumorigenesis

机译：RB1癌症:RB1的不同机制失活和复审委员会的改造途径肿瘤发生

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摘要

Loss of RB1 gene is considered either a causal or an accelerating event in retinoblastoma. A variety of mechanisms inactivates RB1 gene, including intragenic mutations, loss of expression by methylation and chromosomal deletions, with effects which are species-and cell type-specific. RB1 deletion can even lead to aneuploidy thus greatly increasing cancer risk. The RB1gene is part of a larger gene family that includes RBL1 and RBL2, each of the three encoding structurally related proteins indicated as pRb, p107, and p130, respectively. The great interest in these genes and proteins springs from their ability to slow down neoplastic growth. pRb can associate with various proteins by which it can regulate a great number of cellular activities. In particular, its association with the E2F transcription factor family allows the control of the main pRb functions, while the loss of these interactions greatly enhances cancer development. As RB1 gene, also pRb can be functionally inactivated through disparate mechanisms which are often tissue specific and dependent on the scenario of the involved tumor suppressors and oncogenes. The critical role of the context is complicated by the different functions played by the RB proteins and the E2F family members. In this review, we want to emphasize the importance of the mechanisms of RB1/pRb inactivation in inducing cancer cell development. The review is divided in three chapters describing in succession the mechanisms of RB1 inactivation in cancer cells, the alterations of pRb pathway in tumorigenesis and the RB protein and E2F family in cancer.
机译：RB1基因被认为是一个因果或损失一个加速事件在视网膜母细胞瘤。各种机制能灭活RB1基因,包括基因内突变、损失表达式由甲基化和染色体删除,影响洞口细胞的特定类型。非整倍性从而大大增加患癌症的风险。RB1gene是基因家族的一部分包括RBL1和RBL2,三种编码结构相关的蛋白质复审委员会、p107 p130,分别。这些基因和蛋白质源于兴趣他们减缓肿瘤生长的能力。可以与各种蛋白质的吗可以调节许多细胞活动。E2F转录因子家族允许控制的主要功能,而损失这些相互作用大大提高癌症发展。通过不同功能灭活通常组织特定和机制依赖于场景的肿瘤抑制和致癌基因。由不同的上下文是复杂的由RB蛋白和E2F功能家庭成员。强调机制的重要性RB1 /复审委员会在诱导癌症细胞失活发展。连续章节描述的机制在癌细胞的RB1失活,复审委员会通路在肿瘤发生和改变RB蛋白和E2F家族癌症。

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