Relevant studies have indicated the association of HCG18 with tumour occurrence and progression. In this study, we observed that PM 2.5 can enhance the growth of lung adenocarcinoma cells by modulating the expression of HCG18. Further investigations, including overexpression and knockout experiments, elucidated that HCG18 suppresses miR-195, which in turn upregulates the expression of ATG14, resulting in the upregulation of autophagy. Consequently, exposure to PM 2.5 leads to elevated HCG18 expression in lung tissues, which in turn increases Atg14 expression and activates autophagy pathways through inhibition of miR-195, thereby contributing to oncogenesis.
Keyphrases
- poor prognosis
- long non coding rna
- cell proliferation
- signaling pathway
- air pollution
- particulate matter
- induced apoptosis
- cell death
- endoplasmic reticulum stress
- long noncoding rna
- heavy metals
- binding protein
- oxidative stress
- fluorescent probe
- polycyclic aromatic hydrocarbons
- sensitive detection
- transcription factor
- living cells