Abstract
Lung-cancer cell-cycle progression is shaped by interacting checkpoint, transcriptional, chromatin, and non-coding RNA regulatory layers rather than by isolated molecular alterations. This integrative review uses SMARCB1, NOC2L, CDCA4, and CHEK1 as four complementary anchor regulators representing SWI/SNF-dependent chromatin remodeling, inhibition of histone acetyltransferase activity, E2F-linked transcriptional modulation, and checkpoint signaling, respectively. We critically map their literature-supported relationships across G1, S, G2, and M and integrate DNA and histone methylation, acetylation, chromatin remodeling, phosphorylation, ubiquitination, hydroxylation, and non-coding RNA regulation. Importantly, lung-cancer-specific evidence is distinguished from evidence extrapolated from other tumor models, and experimentally established mechanisms are separated from contextual or hypothesis-generating phase assignments. The strongest lung-specific evidence concerns CHEK1 dependence, replication stress, and chromatin-state plasticity, whereas several proposed phase-specific functions of NOC2L, CDCA4, and SMARCB1 remain incompletely validated in lung cancer. Recent 2026 studies further emphasize subtype-specific CHEK1 biology, therapy-associated chromatin reprogramming, and long non-coding RNA control. This framework identifies testable regulatory hypotheses while avoiding interpretation of network association as direct causality.