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Updated: Feb 9, 2026
A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
Published on: July 6, 2017
Expression profile of NF-κB regulated genes in sporadic colorectal cancer patients
Betsy Annel González-Quezada1,2, Uriel Francisco Santana-Bejarano1,2, Alfredo Corona-Rivera1,2
1Cytogenetics and Genomics Laboratory, Human Genetic Institute 'Dr. Enrique Corona Rivera', University of Guadalajara, Guadalajara, Jalisco 44340, México.
Abstract:
Colorectal cancer (CRC) is the fourth leading worldwide cause of cancer-associated mortalities. Nuclear factor-κB (NF-κB) is a transcriptional regulator of multiple genes associated with CRC. Tumor tissue were compared with normal adjacent mucosa from 30 sporadic patients with CRC were investigated. A total of 8 non-CRC patients were analyzed as a control group. In the present study, the protein expression of NF-κB/p65 was detected by immunohistochemistry, and the gene expression profiles of cyclin D1 (CCND1), prostaglandin-endoperoxide synthase 2, vascular endothelial growth factor A, matrix metallopeptidase 9, BCL2 apoptosis regulator (BCL2), BCL2 like 1, nitric oxide synthase 2, tumor necrosis factor and arachidonate lipoxygenase were detected by reverse transcription-quantitative polymerase chain reaction. NF-κB/p65 and genes expression profiles were classified according to tumor-node-metastasis (TNM) clinicopathological parameters, followed by statistical analysis. Higher protein expression of NF-κB/p65 in the cytoplasm of tumor tissues compared with adjacent normal mucosa was reported; this increment was positively associated with all clinicopathological parameters, except for tumor localization site. The selected genes demonstrated a diverse associative pattern when analyzed with clinicopathological parameters. CCND1 was positively associated with all TNM parameters and BCL2 was negatively associated with all TNM parameters, thus indicating their importance as strong molecular biomarkers for CRC. According to these results, not all selected genes regulated by NF-κB/p65 show increased expression during CRC development, whereas the transcription factor did. The present study suggests that NF-κB/p65 overexpression is necessary for CRC establishment and progression, but its transcriptional activity is not sufficient to regulate all target genes in CRC. NF-κB/p65 and the gene expression profiles reported in the present study may be therapeutically useful. Considering the heterogeneity of the disease, the particular evaluation of these molecules may allow for the selection of proper diagnosis, treatment and follow-up for patients with sporadic CRC.
Insights
Nuclear factor-kappa B (NF-κB) overexpression is crucial for colorectal cancer (CRC) development and progression. However, its transcriptional activity doesn't regulate all target genes, highlighting NF-κB and specific gene profiles as potential CRC biomarkers.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide.
- Nuclear factor-kappa B (NF-κB) is implicated in CRC pathogenesis.
- Understanding NF-κB's role and its target genes is crucial for CRC management.
Purpose of the Study:
- To investigate the protein expression of NF-κB/p65 and gene expression profiles in CRC.
- To correlate NF-κB/p65 and target gene expression with clinicopathological parameters.
- To assess the potential of NF-κB/p65 and specific genes as biomarkers for sporadic CRC.
Main Methods:
- Immunohistochemistry to detect NF-κB/p65 protein expression in tumor and adjacent normal tissues.
- Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to analyze gene expression profiles.
- Statistical analysis correlating molecular data with TNM staging.
Main Results:
- Elevated NF-κB/p65 protein expression in CRC tissues compared to normal mucosa.
- NF-κB/p65 expression positively correlated with most clinicopathological parameters.
- Cyclin D1 (CCND1) showed positive association, while BCL2 apoptosis regulator (BCL2) showed negative association with TNM parameters.
Conclusions:
- NF-κB/p65 overexpression is necessary for CRC initiation and progression.
- NF-κB/p65's transcriptional activity is not sufficient to upregulate all its target genes in CRC.
- NF-κB/p65 and specific gene expression profiles may serve as valuable diagnostic and therapeutic biomarkers for sporadic CRC.
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