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Abstract
The innate immune molecule NLR family CARD domain-containing 5 (NLRC5) plays a significant role in endometrial carcinoma (EC) immunosurveillance. However, NLRC5 also plays a protumor role in EC cells. Mismatch repair gene deficiency (dMMR) can enable tumors to grow faster and also can exhibit high sensitivity to immune checkpoint inhibitors. In this study, we attempted to determine whether NLRC5-mediated protumor role in EC is via the regulation of dMMR. Our findings revealed that NLRC5 promoted the proliferation, migration, and invasion abilities of EC cells and induced the dMMR status of EC in vivo and in vitro. Furthermore, the mechanism underlying NLRC5 regulated dMMR was also verified. We first found NLRC5 could suppress nuclear factor-kappaB (NF-κB) pathway in EC cells. Then we validated that the positive effect of NLRC5 in dMMR was restricted when NF-κB was activated by lipopolysaccharides in NLRC5-overexpression EC cell lines. In conclusion, our present study confirmed the novel NLRC5/NF-κB/MMR regulatory mechanism of the protumor effect of NLRC5 on EC cells, thereby suggesting that the NLRC5-mediated protumor in EC was depend on the function of MMR.
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Details
1 The Second Affiliated Hospital of Anhui Medical University, Department of Obstetrics and Gynecology, Hefei, China (GRID:grid.452696.a) (ISNI:0000 0004 7533 3408)
2 The Frist Affiliated Hospital of Anhui Medical University, Department of Obstetrics and Gynecology, Hefei, China (GRID:grid.186775.a) (ISNI:0000 0000 9490 772X)
3 The Second Affiliated Hospital of Anhui Medical University, Department of Oncology, Hefei, China (GRID:grid.452696.a) (ISNI:0000 0004 7533 3408)