BACKGROUND:Firstly, we aimed to compare the differences of higher-order chromatin structure between nasopharyngeal carcinoma (NPC) and normal nasopharyngeal tissues. The second objective was to analyze the specific chromatin interaction site of NPC and the NPC-related genes regulated by this interaction site.METHODS:We included 6 NPC patients and 6 healthy controls to obtain the sequencing results of highest-throughput chromosome conformation capture (Hi-C) technique, followed by further analysis of the specific chromatin interaction sites in NPC.RESULTS:We found an abnormal ultra-long distance interaction site on the chromosome 7p in the CNE210 sample, which was caused by a fusion gene SEPT7P2-PSPH. Additionally, a significant interaction site between chromosome 8q and 3p was revealed in the samples CNE25, CNE29, and CNE211, which was the interaction between 1.5 kb downstream of ASAP1 and 0.8 kb upstream of CTNNB1 gene. Further quantitative polymerase chain reaction (qPCR) revealed that ASAP1 and CTNNB1 genes were more highly expressed in CNE25, CNE29, and CNE211 than in the Np group, preliminarily indicating that this interaction site was likely related to the high expression of ASAP1 and CTNNB1 in NPC.CONCLUSIONS:Through Hi-C analysis, we analyzed the specific chromatin interaction sites associated with NPC, and found the chromosomal translocation and chromatin interaction sites associated with NPC based on statistical analysis. This study has certain guiding significance for in-depth study of the mechanism of NPC occurrence and development.

Epithelial ovarian cancer is one of the most common and aggressive diseases among the female reproductive organ malignancies, and the molecular mechanism underlying this disease remains largely unknown. EMSY, a binding partner of BRCA2, has been reported to be amplified in ovarian cancer. However, the expression pattern and biological functions of EMSY in the progression of ovarian cancer are not fully understood. In this study, it was found that the expression of EMSY was significantly elevated in ovarian cancer samples compared to their adjacent normal tissues. Moreover, overexpression of EMSY promoted the growth and migration of ovarian cancer cells, while knocking down the expression of EMSY inhibited the growth, migration, and tumorigenesis of ovarian cancer cells in vitro and in vivo. Mechanistically, EMSY was found to interact with beta-catenin and activate beta-catenin/TCF signaling. Our study demonstrated that EMSY played an oncogenic role in the progression of ovarian cancer cells and EMSY might be a promising target for the treatment.