Biology ETDs
Publication Date
4-15-2023
Abstract
BRG1 is mutated in 10% of lung cancers, making this mutation clinically relevant. The downstream effects of BRG1 included significantly affecting the cell cycle control and chromosomal replication pathway. CDK18, a cyclin-dependent kinase, was determined to be the gene with significantly decreased expression (p < 0.0001) in the cell cycle control and chromosomal replication pathway. CDK18 is active during the S-phase of the cell cycle and required for genomic stability. Studies were conducted to determine the epigenetic mechanisms that contributed to the repression of CDK18. Histone methylation contributes to the repression of CDK18, and histone deacetylation globally regulates expression of CDK18, while cytosine methylation was found to not contribute to CDK18 expression. Studies were performed to elucidate CDK18 functional role lung carcinogenesis and the genome-wide impact of CDK18 repression. Repression of CDK18 affects cell migration, proliferation, cell-cell signaling, and anchorage-independent growth that contribute to cancer initiation and progression.
Project Sponsors
Lovelace Biomedical Research Institute (RO1 CA196590)
Language
English
Keywords
Cancer, Biology, Epigenetic, Lung, Lung Cancer, BRG1, CDK18, Cell Cycle, Transcription
Document Type
Thesis
Degree Name
Biology
Level of Degree
Masters
Department Name
UNM Biology Department
First Committee Member (Chair)
Christopher A. Johnston
Second Committee Member
Helen J. Wearing
Third Committee Member
Steven A. Belinsky
Recommended Citation
Phillips, Loryn M.. "Transcriptional Silencing of CDK18 and Its Role in Lung Carcinogenesis of BRG1-Mutant Lung Cancers." (2023). https://digitalrepository.unm.edu/biol_etds/380
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Biology Commons, Cancer Biology Commons, Cell Biology Commons