Chlamydia trachomatis upregulates lncRNA CYTOR to mediate autophagy through miR-206/MAPK1 axis.
Shan ChengYi LiuBei HeJinrong ZhangYewei YangXinglv WangZhongyu LiPublished in: Pathogens and disease (2024)
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.
Keyphrases
- signaling pathway
- pi k akt
- cell proliferation
- cell death
- long non coding rna
- oxidative stress
- endoplasmic reticulum stress
- long noncoding rna
- induced apoptosis
- epithelial mesenchymal transition
- poor prognosis
- simultaneous determination
- transcription factor
- infectious diseases
- high throughput
- risk assessment
- solid phase extraction
- single molecule
- combination therapy
- high speed
- smoking cessation