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<p>This study investigated the long non-coding RNA (lncRNA) <i>ESPNP</i> to elucidate its regulatory roles in gastric cancer (GC) cell proliferation, invasion, and metastatic potential. We performed RNA sequencing on gastric cancer liver metastasis (GCLM) tissues, gastric cancer tissues (GCT), and peritumoral tissues (PT) to identify differentially expressed lncRNAs. LncRNA <i>ESPNP</i> was highly expressed in GCLM and GCT, and was thus chosen for further analysis. Cell viability was assessed using the CCK-8 assay, whereas Transwell and wound-healing assays were used to evaluate invasive and migratory capacities. The results revealed that&#xa0;transfection with an <i>ESPNP</i> small interfering RNA (siRNA) significantly suppressed the viability, invasion, and migration of GC cells. Furthermore, compared with transfection with a Twist1 overexpression plasmid alone, co-transfection with the Twist1 plasmid and <i>ESPNP</i> siRNA significantly reduced GC cell viability as well as invasive and migratory capacities. In addition, in vivo experiments demonstrated that <i>ESPNP</i> silencing markedly inhibited tumor growth. Terminal deoxynucleotidyl transferase nick-end-labeling and Ki67 staining also showed that <i>ESPNP</i> short hairpin RNA treatment enhanced cell apoptosis and reduced cell proliferation. Taken together, our study demonstrated that <i>ESPNP</i> promotes GC progression by enhancing proliferation, invasion, metastasis, and epithelial-mesenchyme transition, suggesting its potential as a prognostic biomarker and therapeutic target in GC.</p>

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ESPNP promotes cell migration and invasion in gastric cancer cells via regulation of epithelial-mesenchymal transition/Twist1

  • 期刊论文

  • 发表日期：

    2026年2月19日

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  • Weibing Li,
  • Haiyang Zhang,
  • Xiangyuan Ding,
  • Haining Ma

摘要

This study investigated the long non-coding RNA (lncRNA) ESPNP to elucidate its regulatory roles in gastric cancer (GC) cell proliferation, invasion, and metastatic potential. We performed RNA sequencing on gastric cancer liver metastasis (GCLM) tissues, gastric cancer tissues (GCT), and peritumoral tissues (PT) to identify differentially expressed lncRNAs. LncRNA ESPNP was highly expressed in GCLM and GCT, and was thus chosen for further analysis. Cell viability was assessed using the CCK-8 assay, whereas Transwell and wound-healing assays were used to evaluate invasive and migratory capacities. The results revealed that transfection with an ESPNP small interfering RNA (siRNA) significantly suppressed the viability, invasion, and migration of GC cells. Furthermore, compared with transfection with a Twist1 overexpression plasmid alone, co-transfection with the Twist1 plasmid and ESPNP siRNA significantly reduced GC cell viability as well as invasive and migratory capacities. In addition, in vivo experiments demonstrated that ESPNP silencing markedly inhibited tumor growth. Terminal deoxynucleotidyl transferase nick-end-labeling and Ki67 staining also showed that ESPNP short hairpin RNA treatment enhanced cell apoptosis and reduced cell proliferation. Taken together, our study demonstrated that ESPNP promotes GC progression by enhancing proliferation, invasion, metastasis, and epithelial-mesenchyme transition, suggesting its potential as a prognostic biomarker and therapeutic target in GC.