Objective To observe the curative effect of 8-bromo-7-methoxychrysin (BrMC) on ulcerative colitis associated colorectal cancer (UCAC) mice, and explore the molecular mechanism of BrMC regulation of UCAC mice based on the expression of long non-coding RNA (LncRNA) ELFN1-AS1. Methods The UCAC model of C57BL/6 mice was established by sodium glucan sulfate (DSS) combined with azomethane oxide (AOM), the mice were given BrMC intragastric treatment, and the expression of ELNF1-AS1 in colon tissue was detected by real-time quantitative fluorescence polymerase chain reaction (qRT-PCR). The experiment was divided into 5 groups, including control group, model group, BrMC group, BrMC+NC group, and BrMC+ELFN1-AS1 group, with 10 mice in each group. UCAC model was constructed for the other 4 groups except the control group, BrMC was given intragastric administration or caudal vein injection of ELNF1-AS1 negative control (NC) and overexpressed ELFN1-AS1 plasmid liposome complex. After the administration, the general conditions of mice in each group were observed, body mass and disease activity index (DAI) of mice in each group were determined, pathological injury and tumorigenesis of colon of mice in each group were examined, hematoxylin-eosin (HE) staining was performed to observe the histopathological changes of colon, terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end labeling (TUNEL) was used to detect the apoptosis of colon tissue cells in each group, enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-12 in colon tissue of mice in each group, and the expression levels of ELFN1-AS1 in colon tissue of mice in each group were detected by qRT-PCR. Results The relative expression level of ELFN1-AS1 in colon tissue of mice in model group was significantly up-regulated compared with that in control group (P＜0.05), and the relative expression level of ELFN1-AS1 in colon tissue of mice in BrMC group was significantly down-regulated compared with that in model group (P＜0.05). Further study showed that compared with model group, activity level and mental state of mice in BrMC group were significantly improved, body weight was significantly increased (P＜0.05), DAI score was significantly decreased (P＜0.05), colonic mucosal congestion, edema and ulceration were significantly alleviated, and the number of tumors was significantly reduced (P＜0.05), the damage of epithelial cells and the degree of inflammatory cell infiltration in colon mucosal tissue were decreased, the proportion of TUNEL-labeled apoptotic cells was significantly decreased (P＜0.05), and the levels of TNF-α, IL-1β, IL-6 and IL-12 in colon tissue were significantly decreased (P＜0.05), the relative expression level of ELFN1-AS1 in colon tissues was significantly decreased (P＜0.05). Compared with BrMC group, BrMC+ELFN1-AS1group showed decreased activity and lethargy, body weight significantly decreased (P＜0.05), DAI score was significantly increased (P＜0.05), colonic mucosa was still hyperemia and ulceration, and the number of tumors was significantly increased (P＜0.05), epithelial cells were damaged and infiltrated by inflammatory cells, the number of apoptotic cells with TUNEL labeling was significantly increased (P＜0.05), and the levels of TNF-α, IL-1β, IL-6 and IL-12 in colon tissue were significantly increased (P＜0.05), the relative expression of ELFN1-AS1 in colon tissues was also significantly up-regulated (P＜0.05).Conclusion The abnormal expression of lncRNA ELFN1-AS1 may be related to UCAC in mice, and BrMC can inhibit UCAC by down-regulating lncRNA ELFN1-AS1 expression