Mapping the Epigenetic Regulatory Landscape and Core Transcriptional Axes Across Cell Cycle Phases in Lung Cancer
8 affiliations
- 1Semillero de Investigación—Biología Molecular del Cáncer, Facultad de Medicina, Fundación Universitaria Sanitas, Bogotá 110131, Colombia
- 2Dirección Académica, Universidad Nacional de Colombia, Sede de La Paz, La Paz 111016, Colombia
- 3Grupo de Investigación INPAC, Specialized Laboratory, Clinica Universitaria Colombia, Clínica Colsanitas S.A., Bogotá 111321, Colombia
- 4Grupo de Investigación INPAC, Department of Internal Medicine, Clinica Universitaria Colombia, Clínica Colsanitas S.A., Bogotá 111321, Colombia
- 5Grupo de Investigación INPAC, Facultad de Medicina, Fundación Universitaria Sanitas, Bogotá 110131, Colombia
- 6Grupo de Investigación INPAC, Unidad de Investigación, Fundación Universitaria Sanitas, Bogotá 110131, Colombia
- 7Infectious Diseases Department, Clinica Universitaria Colombia, Clínica Colsanitas S.A., Bogotá 111321, Colombia
- 8Keralty, Sanitas International Organization, Grupo de Investigación INPAC, Fundación Universitaria Sanitas, Bogotá 110131, Colombia
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.
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BibTeX
@article{salcedotuiran2026mapping,
title = {{Mapping the Epigenetic Regulatory Landscape and Core Transcriptional Axes Across Cell Cycle Phases in Lung Cancer}},
author = {Isabella Salcedo-Tuiran and César Payán-Gómez and Juan Javier López-Rivera and Luisa Fernanda Patiño-Unibio and Sally Lorena Arboleda-Mojica and Claudia Aristizábal-Guzmán and Carlos Arturo Álvarez-Moreno and Mario Arturo Isaza-Ruget and Beatriz Andrea Otálora-Otálora},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219992},
url = {https://www.mdpi.com/1422-0067/27/21/9992},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Mapping the Epigenetic Regulatory Landscape and Core Transcriptional Axes Across Cell Cycle Phases in Lung Cancer
AU - Isabella Salcedo-Tuiran
AU - César Payán-Gómez
AU - Juan Javier López-Rivera
AU - Luisa Fernanda Patiño-Unibio
AU - Sally Lorena Arboleda-Mojica
AU - Claudia Aristizábal-Guzmán
AU - Carlos Arturo Álvarez-Moreno
AU - Mario Arturo Isaza-Ruget
AU - Beatriz Andrea Otálora-Otálora
PY - 2026
DA - 2026/11/07
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219992
UR - https://www.mdpi.com/1422-0067/27/21/9992
AB - 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.
SN - 1422-0067
ER -