LncRNA modulates Hippo-YAP signaling to reprogram iron metabolism

Xin-yu He, Xiao Fan, Lei Qu, Xiang Wang, Li Jiang, Ling-jie Sang, Cheng-yu Shi, Siyi Lin, Jie-cheng Yang, Zuo-zhen Yang, Kai Lei, Jun-hong Li, Huai-qiang Ju, Qingfeng Yan, Jian Liu, Fudi Wang, Jianzhong Shao, Yan Xiong, Wenqi Wang () and Aifu Lin ()
Additional contact information
Xin-yu He: Zhejiang University
Xiao Fan: Zhejiang University
Lei Qu: Zhejiang University
Xiang Wang: the First People’s Hospital of Huzhou
Li Jiang: Zhejiang University School of Medicine
Ling-jie Sang: Zhejiang University
Cheng-yu Shi: Zhejiang University
Siyi Lin: Zhejiang University
Jie-cheng Yang: Zhejiang University
Zuo-zhen Yang: Zhejiang University
Kai Lei: Zhejiang University
Jun-hong Li: Zhejiang University
Huai-qiang Ju: Collaborative Innovation Center for Cancer Medicine
Qingfeng Yan: Zhejiang University
Jian Liu: Zhejiang University School of Medicine, Zhejiang University
Fudi Wang: Zhejiang University School of Medicine
Jianzhong Shao: Zhejiang University
Yan Xiong: Zhejiang University
Wenqi Wang: University of California, Irvine
Aifu Lin: Zhejiang University

Nature Communications, 2023, vol. 14, issue 1, 1-17

Abstract: Abstract Iron metabolism dysregulation is tightly associated with cancer development. But the underlying mechanisms remain poorly understood. Increasing evidence has shown that long noncoding RNAs (lncRNAs) participate in various metabolic processes via integrating signaling pathway. In this study, we revealed one iron-triggered lncRNA, one target of YAP, LncRIM (LncRNA Related to Iron Metabolism, also named ZBED5-AS1 and Loc729013), which effectively links the Hippo pathway to iron metabolism and is largely independent on IRP2. Mechanically, LncRIM directly binds NF2 to inhibit NF2-LATS1 interaction, which causes YAP activation and increases intracellular iron level via DMT1 and TFR1. Additionally, LncRIM-NF2 axis mediates cellular iron metabolism dependent on the Hippo pathway. Clinically, high expression of LncRIM correlates with poor patient survival, suggesting its potential use as a biomarker and therapeutic target. Taken together, our study demonstrated a novel mechanism in which LncRIM-NF2 axis facilitates iron-mediated feedback loop to hyperactivate YAP and promote breast cancer development.

Date: 2023
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DOI: 10.1038/s41467-023-37871-5

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