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<p>Inhibitors of apoptosis proteins (IAPs), coded by <i>BIRC</i> genes, are cellular checkpoints that can regulate and inhibit pro-apoptotic caspase signaling. Overexpression of <i>BIRC</i> genes has been associated with cancer progression, multidrug resistance, poor prognosis, and shorter survival in several types of cancer. Using quantitative real-time polymerase chain reaction, we examined the expression of IAP family genes and their regulators: <i>NAIP</i>, <i>BIRC2</i>, <i>BIRC3</i>, <i>XIAP</i>, <i>BIRC5</i>, <i>BIRC6</i>, <i>BIRC7</i>, <i>CASP3</i>, <i>CASP9</i>, <i>DIABLO</i> and <i>XAF1</i>. We also evaluated the impact of clinical parameters (programmed death receptor 1 [PD1] expression, oligodendrocyte transcription factor 2 [Olig2] expression, Ki-67 antigen expression, tumor protein p53 expression in tumor cells, patient survival time, and progression-free survival) on gene expression levels. The expression of <i>BIRC3</i> (<i>p</i> = 0.049), <i>NAIP</i> (<i>p</i> = 0.008), and <i>XAF1</i> (<i>p</i> = 0.032) was significantly higher in tumors negative for Ki67, whereas the remaining genes showed no significant correlation with Ki67 expression. In contrast, <i>BIRC2</i> (<i>r</i>=-0.478 <i>p</i> &lt; 0.05) and <i>BIRC3</i> (<i>r</i>=-0.536 <i>p</i> &lt; 0.05) expression levels were negatively correlated with overall survival. A similar negative association was observed between progression-free survival and the expression of <i>BIRC2</i> (<i>r</i>=–0.481, <i>p</i> &lt; 0.05) and <i>BIRC3</i> (<i>r</i>=-0.540, <i>p</i> &lt; 0.05). To our knowledge, this is the first study to comprehensively assess the relationship between the expression of IAP family genes and their regulators in a homogeneous group of patients diagnosed with pediatric high-grade gliomas (pHGGs). Our findings provide new insights into molecular mechanisms involved in the pathogenesis of pHGGs, however, these preliminary results require confirmation in larger and more detailed studies.</p>

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Reduced expression of BIRC2 and BIRC3 associated with longer survival in pediatric high-grade gliomas

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月30日

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  • Alicja Petniak,
  • Paulina Gil-Kulik,
  • Julia Zarychta,
  • Adrian Kowalczyk,
  • Joanna Trubicka,
  • Marta Perek-Polnik,
  • Cezary Grochowski,
  • Ryszard Maciejewski,
  • Wiesława Grajkowska,
  • Janusz Kocki

摘要

Inhibitors of apoptosis proteins (IAPs), coded by BIRC genes, are cellular checkpoints that can regulate and inhibit pro-apoptotic caspase signaling. Overexpression of BIRC genes has been associated with cancer progression, multidrug resistance, poor prognosis, and shorter survival in several types of cancer. Using quantitative real-time polymerase chain reaction, we examined the expression of IAP family genes and their regulators: NAIP, BIRC2, BIRC3, XIAP, BIRC5, BIRC6, BIRC7, CASP3, CASP9, DIABLO and XAF1. We also evaluated the impact of clinical parameters (programmed death receptor 1 [PD1] expression, oligodendrocyte transcription factor 2 [Olig2] expression, Ki-67 antigen expression, tumor protein p53 expression in tumor cells, patient survival time, and progression-free survival) on gene expression levels. The expression of BIRC3 (p = 0.049), NAIP (p = 0.008), and XAF1 (p = 0.032) was significantly higher in tumors negative for Ki67, whereas the remaining genes showed no significant correlation with Ki67 expression. In contrast, BIRC2 (r=-0.478 p < 0.05) and BIRC3 (r=-0.536 p < 0.05) expression levels were negatively correlated with overall survival. A similar negative association was observed between progression-free survival and the expression of BIRC2 (r=–0.481, p < 0.05) and BIRC3 (r=-0.540, p < 0.05). To our knowledge, this is the first study to comprehensively assess the relationship between the expression of IAP family genes and their regulators in a homogeneous group of patients diagnosed with pediatric high-grade gliomas (pHGGs). Our findings provide new insights into molecular mechanisms involved in the pathogenesis of pHGGs, however, these preliminary results require confirmation in larger and more detailed studies.