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<p>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 <i>PARP1</i> and <i>NF-κB</i> 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.&#xa0;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.</p> Graphical Abstract <p></p>

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Molecular Study of the Poly (ADP-ribose) Polymerase-1 Gene as a Promotor of Inflammation–Driven Colorectal Carcinoma

  • 期刊论文

  • 发表日期：

    2025年6月19日

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  • Eman Hamdey Hamed Aziz,
  • Alshimaa Magdy,
  • Moustafa Abo Zaid,
  • Raymonde Hanna Assaf

摘要

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.

Graphical Abstract