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<p>Breast carcinoma represents the most prevalent form of invasive neoplasia among the female population globally, and is distinguished by its molecular heterogeneity by significant genomic instability. The discipline of bioinformatics provides essential tools for the identification of novel biomarkers and enhances the prospects for subsequent experimental investigations. Differentially expressed messenger RNAs were assembled by employing datasets sourced from the Gene Expression Omnibus repository. Intersection of DEGs and proteins involving in the integrin cell surface interactions were done. Ce-RNA network were constructed and Functional analysis were done. Protein expression analysis, methylation and, Correlation analysis as well as drug sensitivity analysis for the hub genes were performed. The expression of FN1 were evaluated using Real-Time PCR for 45 invasive ductal carcinoma breast tissues and adjacent normal samples. We found FN1, CDH1, COMP, SPP1 and ITGA7 to act in integrin cell surface interactions. The Ce-RNA network consisted of 126 nodes and 192 edges which the network nodes were significantly enriched in known cancer pathways. Protein expressions of FN1, CDH1, COMP was upregulated while ITGA7 were downregulated. The methylation levels in ITGA7 and SPP1 promoter regions were significantly altered across all stages compared to normal. In contrast, FN1 and CDH1 promoter regions exhibited dysregulation only in stage 3 relative to normal. A correlation study identified five positive and three negative gene correlations. Altered expression of FN1, SPP1, CDH1, and ITGA7 in breast cancer enhanced cancer cell susceptibility to specific pharmacological molecules. FN1 expression was markedly higher in breast cancer tissues compared to non-cancerous tissues, showing a threefold increase (p &lt; 0.0001). Both early-stage and advanced-stage cancers showed higher FN1 levels (p = 0.002, p = 0.01). Additionally, FN1 was higher in lower histological grade tissues (p = 0.0002). In ROC curve analysis with limited stage III samples, FN1 showed potential for diagnosing IDC, achieving an AUC of 0.82. We identified FN1 as a highly connected component of integrin cell-surface interactions in breast cancer and provide hypothesis-generating associations with drug sensitivity; these findings require further protein-level validation and functional testing before translational application.</p>

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FN1 as a key gene in modulating the integrin cell surface pathway in breast cancer

  • 期刊论文

  • 发表日期：

    2026年2月25日

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  • Mahboubeh Sadeghi,
  • Abbas Ghaderi,
  • Pegah Mousavi,
  • Soudabeh Sabetian,
  • Amin Ramezani,
  • Mohammad Reza Haghshenas

摘要

Breast carcinoma represents the most prevalent form of invasive neoplasia among the female population globally, and is distinguished by its molecular heterogeneity by significant genomic instability. The discipline of bioinformatics provides essential tools for the identification of novel biomarkers and enhances the prospects for subsequent experimental investigations. Differentially expressed messenger RNAs were assembled by employing datasets sourced from the Gene Expression Omnibus repository. Intersection of DEGs and proteins involving in the integrin cell surface interactions were done. Ce-RNA network were constructed and Functional analysis were done. Protein expression analysis, methylation and, Correlation analysis as well as drug sensitivity analysis for the hub genes were performed. The expression of FN1 were evaluated using Real-Time PCR for 45 invasive ductal carcinoma breast tissues and adjacent normal samples. We found FN1, CDH1, COMP, SPP1 and ITGA7 to act in integrin cell surface interactions. The Ce-RNA network consisted of 126 nodes and 192 edges which the network nodes were significantly enriched in known cancer pathways. Protein expressions of FN1, CDH1, COMP was upregulated while ITGA7 were downregulated. The methylation levels in ITGA7 and SPP1 promoter regions were significantly altered across all stages compared to normal. In contrast, FN1 and CDH1 promoter regions exhibited dysregulation only in stage 3 relative to normal. A correlation study identified five positive and three negative gene correlations. Altered expression of FN1, SPP1, CDH1, and ITGA7 in breast cancer enhanced cancer cell susceptibility to specific pharmacological molecules. FN1 expression was markedly higher in breast cancer tissues compared to non-cancerous tissues, showing a threefold increase (p < 0.0001). Both early-stage and advanced-stage cancers showed higher FN1 levels (p = 0.002, p = 0.01). Additionally, FN1 was higher in lower histological grade tissues (p = 0.0002). In ROC curve analysis with limited stage III samples, FN1 showed potential for diagnosing IDC, achieving an AUC of 0.82. We identified FN1 as a highly connected component of integrin cell-surface interactions in breast cancer and provide hypothesis-generating associations with drug sensitivity; these findings require further protein-level validation and functional testing before translational application.