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E2F1-autophagy-ALDH1A1 axis enhances selfrenewal and drug resistance of lung cancer stem-like cells in a p53-dependent manner by Jingyuan Li1†, Yiyu Chen1†, Jianyu Wang2†, Liyuan Liu1, Javeria Qadir3, Dan Xie1, Xue Wan1, Yanan Luo1, Jiawen Xian1and Ting Ye1* is a book available to read on EtoBox.

What is E2F1-autophagy-ALDH1A1 axis enhances selfrenewal and drug resistance of lung cancer stem-like cells in a p53-dependent manner about?

AbstractLung adenocarcinoma (LUAD) is a predominant subtype of non-small cell lung adenocarcinoma (NSCLC). It is typically asymptomatic and associated with high mortality rates. Despite recent advancements in screening technologies and therapeutic approaches, its pathogenesis still remains elusive. Therefore, it is imperative to explore new diagnostic markers and therapeutic targets for LUAD management. Cancer stem cells (CSCs) have high selfrenewal capacity and incur therapeutic resistance, thus, considered as crucial elements in initiating and promoting tumor development. Contextual to this, the present study reveals the role of the transcriptional activator E2F1 in LUAD oncogenesis and its association with various biological characteristics of lung cancer stem cells (LCSCs). Whereby, it may also serve as a crucial factor in regulating autophagy. Autophagy can modulate stemness by either promoting or inhibiting CSCs characteristics. Pertinently, our study integrated bioinformatics, in-vitro and in-vivo experiments to elucidate that E2F1 can induce ALDH1A1 through autophagy, thus promoting self-renewal and drug resistance of LCSCs, as well as tumorigenicity. Mechanistically, “E2F

Author

Jingyuan Li1†, Yiyu Chen1†, Jianyu Wang2†, Liyuan Liu1, Javeria Qadir3, Dan Xie1, Xue Wan1, Yanan Luo1, Jiawen Xian1and Ting Ye1*

Published

2025

Language

EN