Fig. 6
From: Lung cancer-derived exosomal miR-132-3p contributed to interstitial lung disease development
Inhibition of miR-132-3p abrogated the progression of interstitial lung disease via targeting SPRY1 in NHLF. A The knockdown efficiency of SPRY1 in NHLF was tested by qRT-PCR and Western blot assays. B Cell viabilities were assessed in NHLF transfected with miR-NC, miR-132-3p inhibitor, miR-132-3p inhibitor + sh-NC, and miR-132-3p inhibitor + sh-SPRY1. C Cell colony numbers were detected in all groups. D Flow cytometry analyzed the apoptosis rate in all groups. E The anti-/pro-apoptosis protein expressions were assessed by Western blot assay. F-G The fibrosis/collagen-associated genes (α-SMA, TGF-β1, COL1A1, and COL3A1), and many pro-inflammatory mediators (IL-1β/6/8) mRNA levels, were tested by qRT-PCR assay. Data were presented as mean ± SD of three independent experiments. ***P < 0.001; **P < 0.01