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<p> The pathogenesis of radiation pneumonitis (RP) is complex, involving multiple genetic and molecular factors. Single-nucleotide polymorphisms (SNPs) at specific microRNA gene loci can influence miRNA expression, even affect disease progression. Genotype distribution of rs1347093 in RP and non-RP groups was analyzed, and the underlying mechanism was explored in human pulmonary microvascular endothelial cells (HPMECs). TaqMan SNP genotyping assay was used to complete the genotyping in 545 subjects with lung cancer, of whom 260 had RP and 285 did not. HPMECs were exposed to 15&#xa0;Gy of X-rays to mimic RP in vitro. mRNA levels were measured via RT-qPCR, while cell apoptosis was assessed via flow cytometry assay. Targeting relationship between the miRNA and the gene was ensured via dual luciferase reporter and RIP assay. The composition ratio of rs1347093 CA genotype carriers in RP group exhibited a significant increase in relation to the non-RP group. The risk of developing pneumonia was 1.827 times higher among CA carriers than CC genotype carriers. Rs1347093 CA/AA genotype remained significantly positively associated with RP risk after controlling for confounding factors. The expression of miR-216a-5p in RP patients exhibited genotype-specific expression patterns, with a significant decrease detected in CA/AA genotype carriers. In HPMECs, miR-216a-5p overexpression attenuated X-ray-mediated apoptosis and ICAM-1 release by targeting and sequestering TGFβR2. Rs1347093 may be a potential genetic marker for susceptibility to RP. It may affect the inflammatory imbalance in RP patients by regulating miR-216a-5p expression.</p>

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Rs1347093 polymorphism contributes to radiation pneumonitis in lung cancer patients through regulating miR-216a-5p expression

  • 期刊论文

  • 发表日期：

    2026年7月10日

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  • Wu Luo,
  • Cuifang Liu,
  • Yuejie Dai,
  • Yin Hong,
  • Haibo Zhang

摘要

The pathogenesis of radiation pneumonitis (RP) is complex, involving multiple genetic and molecular factors. Single-nucleotide polymorphisms (SNPs) at specific microRNA gene loci can influence miRNA expression, even affect disease progression. Genotype distribution of rs1347093 in RP and non-RP groups was analyzed, and the underlying mechanism was explored in human pulmonary microvascular endothelial cells (HPMECs). TaqMan SNP genotyping assay was used to complete the genotyping in 545 subjects with lung cancer, of whom 260 had RP and 285 did not. HPMECs were exposed to 15 Gy of X-rays to mimic RP in vitro. mRNA levels were measured via RT-qPCR, while cell apoptosis was assessed via flow cytometry assay. Targeting relationship between the miRNA and the gene was ensured via dual luciferase reporter and RIP assay. The composition ratio of rs1347093 CA genotype carriers in RP group exhibited a significant increase in relation to the non-RP group. The risk of developing pneumonia was 1.827 times higher among CA carriers than CC genotype carriers. Rs1347093 CA/AA genotype remained significantly positively associated with RP risk after controlling for confounding factors. The expression of miR-216a-5p in RP patients exhibited genotype-specific expression patterns, with a significant decrease detected in CA/AA genotype carriers. In HPMECs, miR-216a-5p overexpression attenuated X-ray-mediated apoptosis and ICAM-1 release by targeting and sequestering TGFβR2. Rs1347093 may be a potential genetic marker for susceptibility to RP. It may affect the inflammatory imbalance in RP patients by regulating miR-216a-5p expression.