基因敲除
自噬
E2F1
癌症研究
细胞生长
生物
E2F型
免疫印迹
细胞
细胞生物学
活力测定
细胞周期
细胞培养
基因
细胞凋亡
遗传学
作者
Wenjun Liang,Mingxia Yang,Xiaohua Wang,Yan Qian,Ruichen Gao,Yujia Shi,Xuejun Shi,Lei Shi,Ting Xu,Qian Zhang
标识
DOI:10.2174/0115680096264557231124102054
摘要
BACKGROUND: Autophagy exerts a vital role in the progression of lung squamous cell carcinoma (LUSC). Ubiquitin-specific peptidase 31 (USP31) has recently been found to be involved in the development of a variety of cancers. However, whether USP31 modulates autophagy in LUSC remains unclear. METHODS: cell counting kit 8 (CCK-8) as well as colony formation, demonstrating that USP31-stable knockdown reduced cell viability. RESULTS: Immunofluorescence analysis illustrated that USP31 knockdown blocked the occurrence of LUSC autophagy. Meanwhile, USP31 has been shown to stabilize the expression of E2F transcription factor 1 (E2F1) through the proteasome pathway. Furthermore, overexpressed E2F1 effectively eliminated the effect of USP31 knockdown on LUSC cell proliferation and autophagy. CONCLUSION: In summary, this investigation proved that USP31 promoted LUSC cell growth and autophagy, at least in part by stabilizing E2F1 expression, which provided a potential therapeutic gene for the treatment of LUSC.
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