LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

Abstract

LINC00599 has been reported to be upregulated in response to cigarette smoking. However, the effect and underlying mechanism of LINC00599 in chronic obstructive pulmonary disease (COPD) are still under exploration. In this study, LINC00599 was upregulated in the COPD patients and was of clinical value to distinguish COPD patients. COPD cell models were established using 16HBE cells under cigarette smoke extract (CSE) treatment. LINC00599 levels were elevated in a dose and time-dependent way in response to CSE stimulation. The effect of LINC00599 on CSE-induced 16HBE cells was explored. The results showed that LINC00599 deficiency reversed the CSE-induced inhibition on cell viability and proliferation, and rescued the CSE-induced enhancement on cell 16HBE cell apoptosis and inflammation response. Moreover, LINC00599 bound with miR-212-5p to upregulate the BASP1 (brain abundant membrane attached signal protein 1) expression. MiR-212-5p was expressed at a low level in the tissue samples of COPD patients, and its levels were upregulated in LINC00599 silenced cells. BASP1 was targeted by miR-212-5p and its upregulation was identified in the tissue samples of COPD patients and cell models. BASP1 levels were downregulated after miR-212-5p overexpression or LINC00599 silencing. Moreover, the rescue assays demonstrated that BASP1 overexpression reversed the effect of silenced LINC00599 on 16HBE cells after CSE treatment, which indicated that LINC00599 promoted the COPD development by regulating BASP1 expression. In conclusion, LINC00599 facilitated CSE-induced cell apoptosis and inflammation response, while inhibiting the cell viability and proliferation in COPD progression via modulating miR-212-5p/BASP1 axis.

The utility of long non-coding RNAs in chronic obstructive pulmonary disease: a comprehensive analysis

“…All the included literature were published from 2019 to 2023 and conducted in China, with a total of 2983 participants involved. There were 7 literature [ 13 , 14 , 25 , 26 , 29 , 35 , 36 ] that included AECOPD patients, stable COPD patients, and normal controls (NCs), 7 literature [ 27 , 28 , 31 – 33 , 37 , 38 ] that recruited COPD patients and NCs, and 3 literature [ 15 , 30 , 34 ] that compared AECOPD patients with COPD patients. The specimen sources were mainly plasma, serum, peripheral blood mononuclear cells (PBMCs), and lung tissue.…”

“…The specimen sources were mainly plasma, serum, peripheral blood mononuclear cells (PBMCs), and lung tissue. All 15 lncRNAs involved, 10 lncRNAs were up-regulated ( NEAT1 , NR-026690 , ENST00000447867 , PACER , MALAT1 , PVT1 , OIP5-AS1 , LUCAT1 , MEG3 , LINC00599 ) [ 13 – 15 , 26 , 27 , 29 , 31 , 33 , 35 – 37 ] and 5 were down-regulated ( ANRIL , LINC00987 , Lnc-IL7R , CASC2 , LINC00612 ) [ 25 , 28 , 30 , 32 , 34 , 38 ]. The characteristics of the included literature were summarized in Tables 1 and 2 .…”

“…This is the first meta-analysis on the diagnostic accuracy of lncRNAs for COPD. Our meta-analysis had enrolled 17 literature [ 13 – 15 , 25 – 38 ] through searching multiple electron databases, there are 10 upregulated [ 13 – 15 , 26 , 27 , 29 , 31 , 33 , 35 – 37 ] and 5 downregulated [ 25 , 28 , 30 , 32 , 34 , 38 ]. COPD patients might experience two clinical conditions: stable status and AECOPD [ 3 , 45 ].…”