LncRNA small nucleolar RNA host gene 16 (SNHG16) silencing protects lipopolysaccharide (LPS)-induced cell injury in human lung fibroblasts WI-38 through acting as miR-141-3p sponge.

Long noncoding RNA (LncRNA) small nucleolar RNA host gene 16 (SNHG16) is correlated with cell injuries, including pneumonia. However, its role and mechanism remain vague in pneumonia. The interplay among genes was confirmed by dual-luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay. SNHG16 and sushi domain containing 2 (SUSD2) were upregulated, and miRNA (miR)-141-3p was downregulated in the serum of acute pneumonia patients and lipopolysaccharide (LPS)-challenged human lung fibroblasts WI-38. LPS induced apoptosis, autophagy, and inflammatory response in WI-38 cells, which was significantly attenuated by SNHG16 knockdown and/or miR-141-3p overexpression. Notably, both SNHG16 and SUSD2 were identified as target genes of miR-141-3p. Besides, the suppressive role of SNHG16 knockdown in LPS-induced in WI-38 cells was partially abolished by miR-141-3p silencing, and the similar inhibition of miR-141-3p overexpression was further blocked by SUSD2 restoration. In conclusion, knockdown of SNHG16 could alleviate LPS-induced apoptosis, autophagy, and inflammation in WI-38 cells partially though the SNHG16/miR-141-3p/SUSD2 pathway.