Background <p>LncRNA <i>HOXB-AS3</i> has been shown to exert oncogenic effects in various malignancies. However, its specific role in gastric cancer (GC) remains largely unknown. This study addressed the expression profile and clinical relevance of <i>HOXB-AS3</i> in GC. Moreover, we dissected its downstream regulatory circuitry in a cell model.</p> Methods <p>The cohort comprised 156 GC patients who were followed up for 5 years. Multivariate Cox analysis was employed for risk indicator identification. Relative expression of genes was calculated by RT-qPCR. Cell proliferation was detected by CCK-8 assay, while migration and invasion were assessed by transwell assay. ROC curve was applied for diagnostic efficiency.</p> Results <p><i>HOXB-AS3</i> was upregulated in GC tissues (<i>P</i> &lt; 0.001) and exhibited promising diagnostic utility (AUC = 0.851, 95% CI: 0.810–0.892). Moreover, high <i>HOXB-AS3</i> expression positively correlated with poor prognosis (<i>P</i> = 0.005) and was identified as another risk factor (HR = 1.642, 95%CI:1.054–2.557, <i>P</i> = 0.028) besides TNM stage and lymph node metastasis. Mechanistically, <i>HOXB-AS3</i> overexpression promoted cell proliferation, migration, and invasion through the <i>miR-498-5p/EP300</i> axis in GC cells.</p> Conclusions <p>Our findings establish <i>HOXB-AS3</i> as a potential diagnostic biomarker and therapeutic target in GC, acting via the <i>miR-498-5p/EP300</i> axis.</p>

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Clinical value and regulatory role of lncRNA HOXB-AS3 in gastric cancer

  • Yushuang Ding,
  • Lihong Zhang,
  • Yuan Xu,
  • Meini Cen,
  • Pengfei Li

摘要

Background

LncRNA HOXB-AS3 has been shown to exert oncogenic effects in various malignancies. However, its specific role in gastric cancer (GC) remains largely unknown. This study addressed the expression profile and clinical relevance of HOXB-AS3 in GC. Moreover, we dissected its downstream regulatory circuitry in a cell model.

Methods

The cohort comprised 156 GC patients who were followed up for 5 years. Multivariate Cox analysis was employed for risk indicator identification. Relative expression of genes was calculated by RT-qPCR. Cell proliferation was detected by CCK-8 assay, while migration and invasion were assessed by transwell assay. ROC curve was applied for diagnostic efficiency.

Results

HOXB-AS3 was upregulated in GC tissues (P < 0.001) and exhibited promising diagnostic utility (AUC = 0.851, 95% CI: 0.810–0.892). Moreover, high HOXB-AS3 expression positively correlated with poor prognosis (P = 0.005) and was identified as another risk factor (HR = 1.642, 95%CI:1.054–2.557, P = 0.028) besides TNM stage and lymph node metastasis. Mechanistically, HOXB-AS3 overexpression promoted cell proliferation, migration, and invasion through the miR-498-5p/EP300 axis in GC cells.

Conclusions

Our findings establish HOXB-AS3 as a potential diagnostic biomarker and therapeutic target in GC, acting via the miR-498-5p/EP300 axis.