LncRNA 220, a newly discovered long non-conding RNA inhibiting apoptosis and autophagy in Kupffer cells in LPS-induced endotoxemic mice through the XBP1u-PI3K-AKT pathway

Yang, Ying; Tian, Tian; Wang, Zhenqi; Li, Shan; Li, Nanhong; Luo, Haihua; Jiang, Yong

doi:10.1016/j.intimp.2024.111497

Cited by 1 publication

(1 citation statement)

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“…In the cytoplasm, they act as competitive endogenous RNAs (ceRNAs) to regulate the expression of specific miRNAs, and then target the downstream molecules of miRNA to further regulate the expression of target genes (Fabian and Sonenberg 2012 ). lncRNAs have been confirmed to be key to diverse biological processes, such as apoptosis, metastasis, DNA damage repair processes and autophagy (Wen et al 2020 , Wang et al 2024 , Yadav and Kulshreshtha 2024 ), LncRNA 220 inhibited apoptosis and autophagy through the XBP1u-PI3K-AKT pathway (Yang et al 2024 ) and lncRNA FIRRE induced autophagy to regulated radiotherapy sensitivity (Cai et al 2024 ). Cytoskeleton regulator RNA (CYTOR) can affect the progression of by regulating autophagy (Deng et al 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Chlamydia trachomatis upregulates lncRNA CYTOR to mediate autophagy through miR-206/MAPK1 axis

Cheng,

Liu,

et al. 2024

Pathogens and Disease

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Chlamydia trachomatis infection can be regulated by autophagy-related genes. LncRNA CYTOR has been proven to be involved in autophagy. In this research, we investigated the role of CYTOR in autophagy induced by C. trachomatis and the potential mechanisms. After C. trachomatis infection, CYTOR and MAPK1 were up-regulated and miR-206 was down-regulated, meanwhile, the autophagy-related protein Beclin1 and LC3-Ⅱ/LC3-Ⅰ ratio were increased. Interference with CYTOR or overexpression with miR-206 downregulated the autophagy-related protein Beclin1 and the number of autophagic spots LC3, decreased the protein ratio of LC3-II/LC3-I, and upregulated the expression of P62 protein. The luciferase reporter assay confirmed that CYTOR acted as a sponge for miR-206 to target MAPK1. In addition, CYTOR promoted autophagy induced by C. trachomatis infection through the MAPK1/ERK signaling pathway activation. Taken together, we have identified a novel molecular mechanism that the CYTOR/miR-206/MAPK1 axis was involved in the regulation of autophagy in C. trachomatis infection. This work provides an experimental basis for elucidating the pathogenesis of C. trachomatis for the treatment, prevention and control of related infectious diseases.

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