<scp>C</scp>irc<scp>CCNB</scp>1 inhibits vasculogenic mimicry by sequestering <scp>NF</scp>90 to promote mi<scp>R</scp>‐15b‐5p and mi<scp>R</scp>‐7‐1‐3p processing in nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is a kind of malignant tumor with high metastasis. Circular RNAs (circRNAs) are involved in tumor progression, but their functions and mechanisms are not well understood. Vasculogenic mimicry (VM) has been discovered as an alternative way to supply tumor nutrition and accelerate tumor progression, including NPC. We previously found that circCCNB1 (derived from cyclin B1) could inhibit the migration and invasion of NPC cells by binding to nuclear factor 90 (NF90), however, whether circCCNB1 has additional biological functions is still unclear. In this study, the effects of circCCNB1 binding to NF90 on the generation of miR-15b-5p and miR-7-1-3p were detected using qRT-PCR, western blotting, RNA pulldown, ribonucleoprotein immunoprecipitation and truncated experiments. VM formation assays were used to assess their biological functions. We found that circCCNB1 promoted the processing and generation of miR-15b-5p and miR-7-1-3p through competitive binding to NF90, thereby inhibiting the expression of calumenin (CALU), kinesin family member 1B (KIF1B), RNA polymerase III subunit G (POLR3G), ultimately decreasing the VM of NPC cells. This study not only reveals a new function of circCCNB1 in NPC, but also provides new insights for targeting angiogenesis therapy.