Scholarlink

Background <p>Gastric cancer (GC) prognosis remains poor, necessitating reliable biomarkers. Disulfidptosis represents a promising therapeutic frontier. This study aimed to construct a prognostic model based on disulfidptosis-related LncRNAs (DRLs) and investigate their function.</p> Methods <p>DRLs were screened from TCGA-STAD using Pearson correlation and LASSO-COX regression to build a prognostic signature. Its accuracy was evaluated via Kaplan-Meier analysis, time-dependent ROC curves, and decision curve analysis. A key DRL was functionally validated in vitro and in vivo.</p> Results <p>We established a six-DRL signature (<i>AC090809.1</i>,<i> CYP4A22-AS1</i>,<i> AL356417.2</i>,<i> Z94721.2</i>,<i> FP325313.3</i>,<i> ERICH3-AS1</i>) that effectively stratified patients into risk groups with distinct survival (<i>P</i> &lt; 0.05). The risk score was an independent prognostic factor, with robust predictive AUCs for 1-, 2-, and 3-year survival. AL356417.2 was upregulated in GC and linked to poor outcome. Its knockdown inhibited cell viability, induced F-actin depolymerization, increased cystine uptake, and suppressed tumor growth in mice.</p> Conclusion <p>We developed a novel DRL-based prognostic model and identified AL356417.2 as a functional regulator suppressing disulfidptosis, providing mechanistic insights and a potential therapeutic target for GC.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Constructing and investigating a disulfidptosis-associated LncRNA signature for prognostic prediction in gastric cancer

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月20日

查看全文
  • Namei Li,
  • Zhongyi Tong,
  • Xiaoling She

摘要

Background

Gastric cancer (GC) prognosis remains poor, necessitating reliable biomarkers. Disulfidptosis represents a promising therapeutic frontier. This study aimed to construct a prognostic model based on disulfidptosis-related LncRNAs (DRLs) and investigate their function.

Methods

DRLs were screened from TCGA-STAD using Pearson correlation and LASSO-COX regression to build a prognostic signature. Its accuracy was evaluated via Kaplan-Meier analysis, time-dependent ROC curves, and decision curve analysis. A key DRL was functionally validated in vitro and in vivo.

Results

We established a six-DRL signature (AC090809.1, CYP4A22-AS1, AL356417.2, Z94721.2, FP325313.3, ERICH3-AS1) that effectively stratified patients into risk groups with distinct survival (P < 0.05). The risk score was an independent prognostic factor, with robust predictive AUCs for 1-, 2-, and 3-year survival. AL356417.2 was upregulated in GC and linked to poor outcome. Its knockdown inhibited cell viability, induced F-actin depolymerization, increased cystine uptake, and suppressed tumor growth in mice.

Conclusion

We developed a novel DRL-based prognostic model and identified AL356417.2 as a functional regulator suppressing disulfidptosis, providing mechanistic insights and a potential therapeutic target for GC.