Angiogenesis is a prerequisite process for tumor progression and metastasis in various cancer types, including the cervix. Unlike intact vessels in the physiological state, blood vessels in cervical tumors display a leaky and tortuous phenotype, which impedes the efficiency of anticancer drugs. Hence, over the years, either inhibiting angiogenesis or normalizing the tumor vasculature has been an attractive therapeutic strategy to reduce tumor burden and progression. However, several antiangiogenic drugs do not have enduring effects because of either mutations or the activation of alternate angiogenic pathways. Therefore, identification of the underlying mechanisms regulating cervical tumor angiogenesis may facilitate the development of novel therapeutic strategies. Multiple factors, such as hypoxia, pH, cytokines, and growth factors in the cervical tumor microenvironment (in), activate the epigenome of tumor cells and lead to altered gene expression of proangiogenic molecules, resulting in neovascularization. Chromatin remodeling, an epigenetic mechanism, significantly regulates genes that control tumor angiogenesis. However, the influence of chromatin remodelers and histone modifiers on proangiogenic genes in cervical tumors is not understood. In the present review, we explore the histone modification patterns of the HeLa and SiHa cell lines in the ENCODE database to gain novel insights into the chromatin remodeling of proangiogenic genes in cervical tumors. We show enrichment of genes involved in major angiogenic phases encoding ECM proteins such as COL15A1, ELN, LAMB1, LAMB2, and LAMC1; transcription factors such as RUNX1, SMAD3, HIF1A, GATA2, and XBP1; receptors such as FLT4, TIE1, EPHA2, BMPR2, NOTCH1, CD40, and PPARG; and adhesion molecules such as JUP, ANXA1, ANXA3, GJA5, CDH13, CEACAM1, and THBS1. Taken together, our analysis revealed that cancer cells express numerous proangiogenic genes upon the activation of histone marks, indicating a significant role for chromatin remodeling.