Cancer remains one of the leading causes of death worldwide, and understanding the mechanisms that promote tumor progression can help develop effective therapeutics. A hallmark of many cancers is a deformed nucleus. One common abnormality is nuclear blebbing. Nuclear blebbing refers to a protrusion on the cell’s nucleus, which leads to nuclear rupture and dysfunction. JQ1 is a molecular inhibitor of the bromodomain and extraterminal domain (BET) protein, BRD4, which is important for gene expression in cancer cells, euchromatin maintenance, and cancer progression. Recent research indicates that JQ1 is an effective BET inhibitor with anti-cancer properties. However, how the BRD4 inhibitor JQ1 impacts nuclear blebbing and rupture, a major phenotype of cancer, remains unknown. We performed live-cell imaging to examine nuclear morphology during a day-long treatment with JQ1 and observed a reduction in nuclear blebbing and rupture with JQ1 treatment. To measure levels of decompacted chromatin, an immunofluorescence experiment using the euchromatin marker H3K9ac was used. We found that JQ1 treatment decreased H3K9ac levels, suggesting reduced euchromatin and a more compact chromatin state. The suppression of nuclear blebbing by JQ1 can be attributed to either changes in transcriptional dynamics or euchromatin levels. It remains unclear whether JQ1 suppresses blebbing by altering transcriptional activity or by changing histone modifications that promote chromatin compaction. These experiments provide a connection between transcription regulation and chromatin organization, giving us insight into JQ1’s therapeutic potential to improve nuclear stability in cancer cells.