基因沉默
细胞粘附
癌症研究
小RNA
转移
生物
淋巴系统
细胞迁移
细胞生物学
细胞生长
癌症
细胞
免疫学
基因
生物化学
遗传学
作者
Yinan Zhang,Zhen Feng,Yue Xu,Sufen Jiang,Qianshi Zhang,Zhenyu Zhang,Ke-Yong Wang,Yongming Li,Lijie Xu,Ming Yuan,Zihao Chen,Jingyi Cui,Han Wu,Yina Gao,Wei Wei,Bo Wang,Yunfei Zuo,Shuo Ren
标识
DOI:10.1038/s41419-022-05026-x
摘要
Liver and lymph node sinusoidal endothelial cell C-type lectin (LSECtin) plays an important regulatory role in a variety of diseases, including tumors. However, the underlying mechanism of LSECtin in gastric cancer (GC) remains largely unknown. In our research, LSECtin promoted the adhesion and invasion of GC cells, and was involved in lymphatic metastasis of GC cells. Mechanistically, LSECtin promoted the adhesion, proliferation and migration of GC cells by downregulating STAT1 expression. The circular RNA circFBXL4, which is regulated by LSECtin, sponges the microRNA miR-146a-5p to regulate STAT1 expression. The promotion of GC cell proliferation, migration and invasion mediated by LSECtin was largely inhibited by circFBXL4 overexpression or miR-146a-5p silencing. Moreover, in its role as a transcription factor, STAT1 modulated the expression of FN1 and CHD4. In conclusion, LSECtin might be involved in the lymphatic metastasis of GC by upregulating the expression of FN1 and CHD4 via the circFBXL4/miR-146a-5p/STAT1 axis, possibly indicating a newly discovered pathogenic mechanism.
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