LGR5型
同源盒蛋白纳米
Wnt信号通路
SOX2
癌症干细胞
癌症研究
干细胞
生物
癌细胞
干细胞标记物
癌症
基因敲除
异位表达
下调和上调
KLF4公司
癌变
细胞生物学
细胞培养
胚胎干细胞
信号转导
诱导多能干细胞
生物化学
遗传学
基因
作者
Chuang Wang,Yunhe Gao,Wenying Liang,Yuhan Lu,KeCheng Zhang,Di Wu,ZiWei Zhuang,Kai Li,Zhi Qiao,Hongqing Xi,Lin Chen
标识
DOI:10.1016/j.bbrc.2022.06.002
摘要
Gastric cancer is a one of the most common malignant tumors with poor prognosis worldwide. Leucine-rich G-protein-coupled receptor 5 (LGR5) is determined as a modulator of Wnt signaling cascade and R-spondins are a family of secretory agonists in the Wnt signaling and act as ligands to interact with LGR5. However, the function of Rspondin-1 in GC remains obscure. Here, we identified the effect of Rspondin-1 on GC progression. Rspondin-1 and LGR5 were upregulated in clinical gastric cancer tissues. CCK-8 assay revealed that the viability of GC cells was reduced by Rspondin-1 depletion and enhanced by Rspondin-1 overexpression. The depletion of Rspondin-1 decreased while the overexpression of Rspondin-1 increased the numbers of colony formation and Edu-positive GC cells. The depletion of Rspondin-1 attenuated the invasion and migration ability of GC cells. Moreover, sphere formation assays revealed that the knockdown of Rspondin-1 reduced the stemness of GC cells. The expression of cancer stem cell markers, including Nanog, OCT3/4, and SOX2 were suppressed by Rspondin-1 depletion in GC cells. Rspondin-1 induced tumor growth of gastric cancer cells in vivo. Mechanically, the cell viability and invasion suppressed by the depletion of Rspondin-1 in GC cells were rescued by LGR5 overexpression. Besides, the overexpression of LGR5 reversed Rspondin-1 knockdown-inhibited Nanog and OCT3/4 expression. Consequently, we concluded that Rspondin-1 contributes to the progression and stemness of gastric cancer by LGR5.
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