G1 cell cycle phase dynamics are regulated by intricate networks involving cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors, which control G1 progression and ensure proper cell cycle transitions. Moreover, adequate origin licensing in G1 phase, the first committed step of DNA replication in the subsequent S phase, is essential to maintain genome integrity. In this review, we highlight the intriguing parallels and disparities in G1 dynamics between stem cells and cancer cells, focusing on their regulatory mechanisms and functional outcomes. Notably, SOX2, OCT4, KLF4, and the pluripotency reprogramming facilitator c-MYC, known for their role in establishing and maintaining stem cell pluripotency, are also aberrantly expressed in certain cancer cells. In this review, we discuss recent advances in understanding the regulatory role of these pluripotency factors in G1 dynamics in the context of stem cells and cancer cells, which may offer new insights into the interconnections between pluripotency and tumorigenesis.
G1期细胞周期动态受复杂网络调控，该网络涉及细胞周期蛋白、细胞周期蛋白依赖性激酶（CDKs）及其抑制因子，共同控制G1期进程并确保细胞周期的正常转换。此外，G1期充分的复制起点许可作为后续S期DNA复制的首个关键步骤，对维持基因组完整性至关重要。本综述重点探讨干细胞与癌细胞在G1期动态调控中引人注目的相似性与差异性，聚焦其调控机制及功能结果。值得注意的是，SOX2、OCT4、KLF4以及多能性重编程促进因子c-MYC在建立和维持干细胞多能性中发挥关键作用，同时也在某些癌细胞中异常表达。本文讨论了这些多能性因子在干细胞和癌细胞G1期动态调控作用的最新研究进展，这可能为理解多能性与肿瘤发生之间的内在联系提供新视角。
肿瘤(癌症)患者之家