Aziz Eman Hamdey Hamed, Magdy Alshimaa, Abo Zaid Moustafa, Assaf Raymonde Hanna
Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Gastroenterology Surgical Center, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Biochem Genet. 2025 Jun 19. doi: 10.1007/s10528-025-11159-3.
Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related deaths worldwide. Chronic inflammation is a risk factor for various cancers, including CRC. However, the specific mechanisms by which inflammation contributes to cancer development are not fully understood. Our study assessed PARP1 and NF-κB mRNA expression in different stages of CRC, aiming to elucidate their roles in inflammation-driven CRC pathogenesis and define their stage-specific expression patterns. The study involved 35 CRC tissue samples and a control group of 25 samples from the healthy margins of colon cancer. PARP1 and NF-κB mRNA levels were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in tumor tissue samples, as well as the adjacent part of normal tissue. Our results revealed that PARP1 and NF-κB/p50 gene expression was significantly higher in CRC vs. control. Furthermore, there was a positive correlation between PARP1 and NF-κB/p50 mRNA expression levels. PARP1 was found to be responsible for 14.5% of the change in NF-κB/p50. Both PARP1 and NF-κB/p50 had high accuracy in the diagnosis of CRC with AUC = 0.905 and 0.956, respectively. This study revealed the overexpression of PARP1 and NF-κB genes in CRC cases, which suggests that the use of PARP1 inhibitors and anti-inflammatory drugs could be effective in CRC treatment. PARP1/NF-κB showed preliminary associations with CRC that merit diagnostic evaluation in larger studies. Our data suggest that PARP1 and NF-κB expression may complement CEA in characterizing CRC biology though future studies must determine whether these markers have independent prognostic value.
结直肠癌（CRC）是全球第三大常见癌症，也是癌症相关死亡的第二大主要原因。慢性炎症是包括CRC在内的各种癌症的一个危险因素。然而，炎症促进癌症发展的具体机制尚未完全明确。我们的研究评估了PARP1和NF-κB mRNA在CRC不同阶段的表达，旨在阐明它们在炎症驱动的CRC发病机制中的作用，并确定它们的阶段特异性表达模式。该研究纳入了35个CRC组织样本和一个由25个来自结肠癌健康边缘组织样本组成的对照组。通过逆转录定量聚合酶链反应（RT-qPCR）测定肿瘤组织样本以及正常组织相邻部分的PARP1和NF-κB mRNA水平。我们的结果显示，与对照组相比，CRC中PARP1和NF-κB/p50基因表达显著更高。此外，PARP1和NF-κB/p50 mRNA表达水平之间存在正相关。发现PARP1可解释NF-κB/p50变化的14.5%。PARP1和NF-κB/p50在CRC诊断中均具有较高准确性，AUC分别为0.905和0.956。本研究揭示了CRC病例中PARP1和NF-κB基因的过表达，这表明使用PARP1抑制剂和抗炎药物可能对CRC治疗有效。PARP1/NF-κB与CRC显示出初步关联，值得在更大规模研究中进行诊断评估。我们的数据表明，PARP1和NF-κB表达可能在表征CRC生物学方面补充癌胚抗原（CEA），不过未来研究必须确定这些标志物是否具有独立的预后价值。
