Carcinogenic transformation of somatic cells resembles nuclear reprogramming toward the generation of pluripotent stem cells. These events share eternal escape from cellular senescence, continuous self-renewal in limited but certain population of cells, and refractoriness to terminal differentiation while maintaining the potential to differentiate into cells of one or multiple lineages. As represented by several oncogenes those appeared to be first keys to pluripotency, carcinogenesis and nuclear reprogramming seem to share a number of core mechanisms. The retinoblastoma tumor suppressor product retinoblastoma (RB) seems to be critically involved in both events in highly complicated manners. However, disentangling such complicated interactions has enabled us to better understand how stem cell strategies are shared by cancer cells. This review covers recent findings on RB functions related to stem cells and stem cell-like behaviors of cancer cells.

中文翻译：

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干细胞和癌细胞策略共享视网膜母细胞瘤肿瘤抑制功能。


体细胞的致癌转化类似于核重编程以产生多能干细胞。这些事件的共同特点是永远逃避细胞衰老、在有限但特定的细胞群中持续自我更新、难以终末分化，同时保持分化成一种或多种谱系细胞的潜力。以几种癌基因为代表，这些癌基因似乎是多能性的首要关键，癌发生和核重编程似乎共享许多核心机制。视网膜母细胞瘤肿瘤抑制产物视网膜母细胞瘤（RB）似乎以高度复杂的方式与这两个事件密切相关。然而，解开这种复杂的相互作用使我们能够更好地理解癌细胞如何共享干细胞策略。这篇综述涵盖了与干细胞相关的 RB 功能和癌细胞的干细胞样行为的最新发现。