The expression of NONO, ERG, or Ets-1 is associated with poor outcome of gastric cancer patients. a Representative immunohistochemical staining images showing the nuclear and cytoplasmic expression pattern of NONO, ERG, and Ets-1 in normal gastric mucosa, precancerous gastric mucosa, and tumor cells of gastric cancer specimens (arrowheads, brown). Scale bars: 100 μm. b Western blot assay indicating the differential levels of NONO, ERG, and Ets-1 in normal gastric mucosa (N, n = 30), precancerous tissues (P, n = 81), and gastric cancer tissues (c, n = 81). c Real-time qRT-PCR showing the expression levels (normalized to β-actin) of NONO and ERG in normal gastric mucosa (n = 30), gastric cancer tissues (n = 81), and gastric cancer specimens with (n = 22) or without metastasis (n = 59). d Real-time qRT-PCR assay revealing the NONO and ERG transcript levels (normalized to β-actin) in normal gastric mucosa (n = 30) and cultured gastric cancer cell lines (mean ± SD, n = 5). e The positive correlation between ERG and Ets-1 transcript levels in gastric cancer tissues (n = 81). f Kaplan–Meier curves indicating overall (OS) and first progression (FP) survival of gastric cancer patients derived from Kaplan-Meier plotter with low or high expression of NONO (cutoff values = 7825.0 and 7797.0), ERG (cutoff values = 225.0 and 126.0), or Ets-1 (cutoff values = 126.0 and 89.0). g The mechanisms underlying pancEts-1-drived progression of gastric cancer: as a novel lncRNA, pancEts-1 interacts with NONO to facilitate the physical interaction between NONO and ERG, resulting in transactivation of ERG and transcription of Ets-1 that are associated with gastric cancer progression. Student’s t test analyzed the difference in c and d. Pearson’s correlation coefficient analysis in e. Log-rank test for survival comparison in f