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Background <p>Cancer remains a leading cause of mortality worldwide, posing a serious threat to public health. The ASPN protein has emerged as a key player in certain cancers; however, its precise mechanisms and regulatory roles are still not well-defined.</p> Methods <p>We explored the expression of <i>ASPN</i> and its prognostic significance across various cancers. Functional enrichment analyses were conducted using the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). The association between ASPN expression and factors including immune cell infiltration, immune checkpoint genes, microsatellite instability (MSI), tumor mutational burden (TMB), drug sensitivity, promoter methylation, and tumor mutation types was examined. Finally, the function of ASPN in stomach adenocarcinoma (STAD) was examined using RT-qPCR, WB, Cell Counting Kit-8, Transwell, scratch, and flow cytometry assays, focusing on the effects of ASPN on cell proliferation, migration, invasion, and apoptosis.</p> Results <p><i>ASPN</i> expression was high in several cancers, where higher expression correlated with poorer prognosis. Gene enrichment analysis indicates ASPN is involved in several cellular pathways and correlates with immune cells infiltration, TMB, and MSI. The single-cell analysis showed that ASPN was mainly expressed in fibroblasts, and <i>ASPN</i> mutations predominantly consisted of missense mutations. After using siRNA knockdown of ASPN, CCK-8 assay and wound healing assays exhibited that suppressed cell viability and migration ability of gastric cells, Transwell assay displayed migration and invasion abilities of two gastric cell lines was decreased. In accordance with the result of cell apoptosis, reducing ASPN elevated the rate of apoptosis in two gastric cancer cells. ASPN inhibition leads to upregulation of pro-apoptotic BAX and cleaved Caspase-3, and downregulation of anti-apoptotic BCL2. These findings suggest that ASPN contributes to gastric cancer aggressiveness.</p> Conclusion <p>Elevated ASPN expression across cancers is associated with poorer prognosis, highlighting its potential as a prognostic biomarker and therapeutic target, particularly in gastric cancer.</p>

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Exploring ASPN as a pan-cancer biomarker with a focus on gastric cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月19日

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  • Yue Feng,
  • Sijiang Zhou,
  • Bing Yang,
  • Jian Yang,
  • Shengyu Wang,
  • Zhu Yu,
  • Chao Quan,
  • Junqiang Chen

摘要

Background

Cancer remains a leading cause of mortality worldwide, posing a serious threat to public health. The ASPN protein has emerged as a key player in certain cancers; however, its precise mechanisms and regulatory roles are still not well-defined.

Methods

We explored the expression of ASPN and its prognostic significance across various cancers. Functional enrichment analyses were conducted using the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). The association between ASPN expression and factors including immune cell infiltration, immune checkpoint genes, microsatellite instability (MSI), tumor mutational burden (TMB), drug sensitivity, promoter methylation, and tumor mutation types was examined. Finally, the function of ASPN in stomach adenocarcinoma (STAD) was examined using RT-qPCR, WB, Cell Counting Kit-8, Transwell, scratch, and flow cytometry assays, focusing on the effects of ASPN on cell proliferation, migration, invasion, and apoptosis.

Results

ASPN expression was high in several cancers, where higher expression correlated with poorer prognosis. Gene enrichment analysis indicates ASPN is involved in several cellular pathways and correlates with immune cells infiltration, TMB, and MSI. The single-cell analysis showed that ASPN was mainly expressed in fibroblasts, and ASPN mutations predominantly consisted of missense mutations. After using siRNA knockdown of ASPN, CCK-8 assay and wound healing assays exhibited that suppressed cell viability and migration ability of gastric cells, Transwell assay displayed migration and invasion abilities of two gastric cell lines was decreased. In accordance with the result of cell apoptosis, reducing ASPN elevated the rate of apoptosis in two gastric cancer cells. ASPN inhibition leads to upregulation of pro-apoptotic BAX and cleaved Caspase-3, and downregulation of anti-apoptotic BCL2. These findings suggest that ASPN contributes to gastric cancer aggressiveness.

Conclusion

Elevated ASPN expression across cancers is associated with poorer prognosis, highlighting its potential as a prognostic biomarker and therapeutic target, particularly in gastric cancer.