lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150-5p/SLC38A1 axis
Yanni Yang, Wenlin Tai, Nihong Lu, Ting Li, Yongjun Liu, Wenjuan Wu, Zhengkun Li, Lin Pu, Xiaoyuan Zhao, Tao Zhang, Zhaoxing Dong
Abstract
experiments showed that inhibition of lncRNA ZFAS1 abolished BLM-induced lipid peroxidation and PF development. Mechanistically, silencing of lncRNA ZFAS1 attenuated ferroptosis and PF progression by lncRNA ZFAS1 acting as a competing endogenous RNA (ceRNA) and sponging miR-150-5p to downregulate SLC38A1 expression. Collectively, our studies demonstrated the role of the lncRNA ZFAS1/miR-150-5p/SLC38A1 axis in the progression of PF, and may provide a new biomarker for the treatment of PF patients.
Topics & Concepts
MyofibroblastFibroblastCompeting endogenous RNATransition (genetics)LungCell biologymicroRNABiologyMedicinePathologyCell cultureDownregulation and upregulationInternal medicineGeneticsGeneFibrosisLong non-coding RNACancer-related molecular mechanisms researchRNA modifications and cancerCancer-related gene regulation