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The cell cycle progression pathway encompasses a network of protein kinases (most notably cyclin-dependent kinases—CDKs), regulatory cyclins, transcription factors (particularly E2F), tumor suppressors like the Retinoblastoma protein, and upstream growth factor signaling pathways (e.g., Ras/MAPK, PI3K/Akt) that together orchestrate the ordered progression through cell cycle phases and enforce checkpoint integrity[1][2][3][4][5]. These pathways ensure accurate DNA replication and division and respond to intracellular and extracellular cues. Their disruption—via mutation, deregulation, or exogenous targeting—can lead to uncontrolled proliferation (cancer), genomic instability, or drug resistance[2][3][4][5]. Consequently, individual elements of the cell cycle progression machinery, such as CDKs, cyclins, Rb, or Chk1, are established therapeutic targets in oncology, often with significant challenges regarding specificity and toxicity[2][3][4][5].
Inhibition of cyclin-dependent kinases (preventing phosphorylation events needed for progression through cycle phases); Stabilization or activation of checkpoint kinases (e.g., Chk1); Modulation of tumor suppressor activity (e.g., enhancing Rb repression)
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