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Background <p>Prostate cancer (PCa) is a prevalent urological malignancy. The integrin-linked kinase (<i>ILK</i>) gene has been identified as an oncogenic driver in hormonal cancers, including PCa.</p> Methods <p>To identify key genes in PCa, we utilized differential gene expression analysis and Weighted Gene Co-expression Network Analysis (WGCNA). The ILK gene was silenced using short interfering RNA (siRNA), and subsequent experiments focusing on cellular functionality were conducted to evaluate its impact on cell proliferation, apoptosis, and cell cycle. We examined the expression of autophagy-related and cell cycle-related proteins, including <i>MAP1LC3A, BECN1, C-MYC, TP53,</i> and <i>MDM2</i>. Moreover, we conducted Mfuzz expression pattern clustering analysis, gene set enrichment analysis (GSEA), immune function analysis, transcription factor (TF) analysis, and drug prediction.</p> Results <p>544 significant genes were identified by WGCNA. The protein–protein interaction (PPI) network analysis revealed that MYC was the central regulatory gene, with the intersected genes mainly involved in regulating cell adhesion and drug metabolism in prostate cancer (PCa). Experimental results showed LNCaP cell proliferation was significantly inhibited in the knockdown groups (P &lt; 0.001). Moreover, <i>ILK</i> silencing increased apoptosis in LNCaP cells compared to normal cells and empty vectors, and transfected LNCaP cells were arrested in the S phase of the cell cycle. Notably, C-MYC expression decreased following <i>ILK</i> silencing. Subsequently, we further identified <i>ILK</i>-related regulatory biomarkers.</p> Conclusions <p>The <i>ILK</i> is an oncogene mainly through influencing the <i>C-MYC</i> in PCa. Inhibition of <i>ILK</i> expression would be a promising method for treating the development and progression of PCa.</p>

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Bioinformatics analysis combined with experimental validation reveals the biological role of the ILK gene in prostate cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月31日

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  • Xiao-xiang Yu,
  • Yi Liu,
  • Rong-jiang Luo,
  • Zi-xuan Song,
  • Wen-kai Chen,
  • Zeng-mi Mo,
  • Feng-jing Wang

摘要

Background

Prostate cancer (PCa) is a prevalent urological malignancy. The integrin-linked kinase (ILK) gene has been identified as an oncogenic driver in hormonal cancers, including PCa.

Methods

To identify key genes in PCa, we utilized differential gene expression analysis and Weighted Gene Co-expression Network Analysis (WGCNA). The ILK gene was silenced using short interfering RNA (siRNA), and subsequent experiments focusing on cellular functionality were conducted to evaluate its impact on cell proliferation, apoptosis, and cell cycle. We examined the expression of autophagy-related and cell cycle-related proteins, including MAP1LC3A, BECN1, C-MYC, TP53, and MDM2. Moreover, we conducted Mfuzz expression pattern clustering analysis, gene set enrichment analysis (GSEA), immune function analysis, transcription factor (TF) analysis, and drug prediction.

Results

544 significant genes were identified by WGCNA. The protein–protein interaction (PPI) network analysis revealed that MYC was the central regulatory gene, with the intersected genes mainly involved in regulating cell adhesion and drug metabolism in prostate cancer (PCa). Experimental results showed LNCaP cell proliferation was significantly inhibited in the knockdown groups (P < 0.001). Moreover, ILK silencing increased apoptosis in LNCaP cells compared to normal cells and empty vectors, and transfected LNCaP cells were arrested in the S phase of the cell cycle. Notably, C-MYC expression decreased following ILK silencing. Subsequently, we further identified ILK-related regulatory biomarkers.

Conclusions

The ILK is an oncogene mainly through influencing the C-MYC in PCa. Inhibition of ILK expression would be a promising method for treating the development and progression of PCa.