• Decreased Expression of BTG1 in Colorectal Cancer Tumor Tissue Compared to Adjacent Normal Tissue: Implications for Tumor Progression
  • Yousef Paridar,1 Farhad Ahmadi,2 Mohammad Hossein Shayanpour,3 Moeen Dabirian,4 Maysam Mard-Soltani,5,* Neda Shakerian,6
    1. Gastroenterology Clinic, Dezful University of Medical Sciences, Dezful, Iran
    2. Student Research Committee, Dezful University of Medical Sciences, Dezful, Iran.
    3. Student Research Committee, Dezful University of Medical Sciences, Dezful, Iran.
    4. Student Research Committee, Dezful University of Medical Sciences, Dezful, Iran.
    5. Department of Clinical Biochemistry, Faculty of Medical Sciences, Dezful University of Medical Sciences, Dezful, Iran
    6. Department of Clinical Biochemistry, Faculty of Medical Sciences, Dezful University of Medical Sciences, Dezful, Iran


  • Introduction: Colorectal cancer (CRC) is one of the most common malignancies worldwide, representing nearly 10% of all new cancer cases. It is a major cause of cancer-related deaths globally. The progression of CRC, including its invasion and metastasis, significantly influences clinical outcomes, survival rates, and the overall quality of life for affected patients. As such, identifying the molecular mechanisms and key targets responsible for CRC invasion and metastasis is critical in developing new therapeutic strategies. One of the genes of interest is B-cell translocation gene 1 (BTG1), a member of the TOB/BTG protein family, which has been shown to regulate cell proliferation, apoptosis, and the cell cycle. Previous studies suggest that BTG1 may play an essential role in inhibiting tumor development and progression through its involvement in various cellular processes such as DNA repair, transcriptional regulation, and cell division. BTG1 has been linked to several cancers, including gastric, kidney, liver, breast, and lung cancers, where it has been observed to have abnormal expression levels. The role of BTG1 in colorectal cancer, however, remains underexplored. Given the importance of BTG1 in regulating cellular processes related to cancer progression, this study aims to assess BTG1 gene expression in tumor tissues and adjacent normal tissues from patients with colorectal cancer, focusing on its potential role in CRC progression.
  • Methods: This study was conducted on a cohort of colorectal cancer patients, with samples collected from both tumor tissue and adjacent non-tumor tissue. Total RNA was extracted using standard protocols, and complementary DNA (cDNA) synthesis was performed. Quantitative Real-Time PCR (qRT-PCR) was used to measure the expression of BTG1. Primers specific for BTG1 were designed to span the exon-exon junction to ensure specificity. GAPDH was used as the reference gene for normalization of expression data. The qRT-PCR reactions were performed using SYBR Green Master Mix in a LightCycler® 96 system. The relative expression levels of BTG1 were calculated using the ΔΔCt method, and comparisons between tumor and adjacent normal tissues were made. Statistical analysis was performed using SPSS v.16, and results were presented as mean ± standard deviation. Non-parametric tests, including the Mann-Whitney U test, were used for comparing BTG1 expression between the two tissue types, as the data were not normally distributed. A p-value of less than 0.05 was considered statistically significant.
  • Results: Our findings indicate a significant reduction in BTG1 expression in colorectal cancer tumor tissues compared to the adjacent normal tissues. The expression levels of BTG1 were markedly lower in the tumor samples, with a statistically significant difference observed between the two groups (p < 0.05). These results suggest that downregulation of BTG1 is a characteristic feature of colorectal cancer. Given BTG1's role as an anti-proliferative gene that promotes apoptosis and regulates the cell cycle, the decreased expression observed in CRC tumor tissues may be associated with uncontrolled cellular proliferation and reduced apoptosis, which are hallmarks of cancer progression. Furthermore, BTG1’s involvement in processes such as DNA repair and transcriptional regulation may be impaired in colorectal cancer, contributing to genomic instability and enhanced tumorigenic potential.
  • Conclusion: The results of this study highlight the potential tumor-suppressive role of BTG1 in colorectal cancer. The significant reduction in BTG1 expression in CRC tumor tissues, compared to adjacent normal tissues, suggests that loss of BTG1 function may contribute to colorectal cancer development and progression. Previous studies in other cancers have demonstrated similar downregulation of BTG1, further supporting its role as a tumor suppressor gene across different cancer types. BTG1's involvement in key cellular processes such as DNA repair, cell cycle regulation, and apoptosis underscores its importance in maintaining cellular homeostasis. Loss of BTG1 function may result in disrupted regulation of these processes, leading to increased cellular proliferation, resistance to apoptosis, and enhanced tumor progression in colorectal cancer. Moreover, BTG1’s influence on vascular endothelial growth factor (VEGF) expression and tumor neovascularization may also play a role in CRC metastasis. This study provides evidence for the downregulation of BTG1 in colorectal cancer, highlighting its potential role as a tumor suppressor gene. The reduced expression of BTG1 in tumor tissues suggests that it may be involved in regulating cellular processes that prevent tumor progression. Further research is needed to explore the molecular mechanisms underlying BTG1’s role in colorectal cancer and its potential as a therapeutic target. Targeting BTG1-related pathways may offer new avenues for developing treatment strategies aimed at limiting tumor growth and metastasis in colorectal cancer.
  • Keywords: Colorectal cancer, BTG1, gene expression, qRT-PCR.