生物
基因敲除
SOX4型
癌症研究
细胞生长
干细胞
细胞
癌症干细胞
细胞生物学
细胞培养
肺癌
病理
基因表达
医学
基因
遗传学
发起人
作者
Yiyang Liu,Li Ding,Chunwei Li,Heng Lei,Jianjun Chen,Yulong Hou
出处
期刊:Tissue & Cell
[Elsevier]
日期:2023-12-01
卷期号:85: 102250-102250
被引量:1
标识
DOI:10.1016/j.tice.2023.102250
摘要
Non-small cell lung cancer (NSCLC) is a malignant tumor with extremely high mortality. Uroplakin1B (UPK1B) promotes the occurrence and development of multiple types of cancer by enhancing the expression of c-myc and Sox4. However, whether UPK1B can modulate the development of NSCLC by regulating c-myc/Sox4 axis is unclear. In this study, UPK1B was overexpressed or knocked down in the non-small cell lung cancer cells (NSCLCs) were. Next, the proliferation and invasion of those cells were detected with the EdU staining and transwell assays. Sphere formation assays was performed to examine the stem cell characteristics of those cells. Then, we overexpressed the Sox4 in UPK1B knockdown cells and determined the proliferation and invasion of those cells. Our results showed that UPK1B promoted the proliferation, invasion and stem cell characteristics of NSCLCs. In addition, UPK1B enhanced the expression of c-myc, Sox4 and stem cell associated proteins in those cells. Overexpression of Sox4 rescued the proliferation and invasion of NSCLCs, which were suppressed by the UPK1B knockdown. In summary, our study suggested that UPK1B enhanced the invasiveness and stem cell characteristics of NSCLCs by activating c-myc/UPK1B axis.
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