mir-3180-5p作为新近发现的miRNA，在肿瘤中尚未见报道。前期研究发现，mir-3180-5p在子宫内膜癌细胞和组织中表达下降。初步功能和机制研究表明， mir-3180-5p受P53转录激活而靶击NAP1L1，抑制STAT3信号通路，从而抑制子宫内膜癌的增殖。进一步，我们发现NAP1L1能够通过与HDGF相互结合募集SUMO，竞争性抑制PIAS3与SUMO相互结合，从而抑制PIAS3/SUMO介导的STAT3的降解，最终发挥促进子宫内膜癌增殖的作用。因此，我们的研究将阐明，受P53转录激活的mir-3180-5p通过靶向抑制NAP1L1，减少NAP1L1/HDGF复合物对SUMO的募集，从而竞争性诱导PIAS3/SUMO复合物降解STAT3，抑制子宫内膜癌增殖的分子机制，为探索子宫内膜癌的发生发展提供新的线索。

As a newly discovered miRNA, mir-3180-5p has not been reported in tumors. Previous studies have found that mir-3180-5p expression is reduced in endometrial cancer cells and tissues. Preliminary functional and mechanism studies have shown that mir-3180-5p is activated by P53 transcription and targets NAP1L1, inhibits the STAT3 signaling pathway, and thus inhibits the proliferation of endometrial cancer. Further, we found that NAP1L1 can recruit SUMO by combining with HDGF, competitively inhibit PIAS3 and SUMO from combining with each other, thereby inhibiting PIAS3 / SUMO-mediated degradation of STAT3, and finally play a role in promoting the proliferation of endometrial cancer. Therefore, our study will clarify that mir-3180-5p, which is activated by P53 transcription, inhibits the recruitment of SUMO by the NAP1L1 / HDGF complex by targeting inhibition of NAP1L1, thereby competitively inducing the degradation of STAT3 by the PIAS3 / SUMO complex and inhibiting the uterus. The molecular mechanism of membrane cancer proliferation provides new clues for exploring the occurrence and development of endometrial cancer.