Exposure to ultraviolet radiation (UVR) is a principal cause of keratinocyte skin cancers in humans. Brm (Brahma) is a chromatin remodelling protein belonging to the SWI/SNF complex, whose loss is associated with keratinocyte skin cancers. Previously, we showed that Brm expression is reduced during the progression from actinic keratoses to cutaneous squamous cell carcinomas (CSCCs) in humans, and that its loss in UV-irradiated mouse skin leads to epidermal hyperplasia and an increased tumour incidence. In this study, we identified the roles of Brm in keratinocyte responses to UVR-induced DNA damage. In both neonatal mouse keratinocytes and the human keratinocyte cell line, HaCaT, the loss of Brm expression led to an increased proliferation following exposure to UVR. Cell cycle analysis showed that this was due to a reduced time spent in G1 cell cycle arrest. Furthermore, Brm-deficient cells displayed an increased formation of UVR-induced DNA photolesions. It was found that primary neonatal keratinocytes harbouring Brm loss were more sensitive to UVR. This may have been due to these cells being naïve, whereas HaCaT cells already exhibit several UVR-induced mutations, such as that of p53. The loss of Brm in combination with UVR was sufficient to cause increased cellular sensitivity to UVR, leading to the proliferation of cells whilst harbouring DNA photolesions, as well via defective G1 cycle checkpoints, leading to increased numbers of S and M-phase cells. This would likely lead to heightened levels of mutations in the cell, and increased carcinogenesis downstream, as previously witnessed in Brm-deficient mice.