Ehab Maher - Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt
Gamalat Gedawy - Department of Clinical Biochemistry and Molecular Diagnostic, National Liver Institute, Menofyia University, Sebin El-Kom, Egypt
Walid Fathy - Department of Clinical Pathology, Faculty of Medicine, Menofyia University, Sebin El-Kom, Egypt
Sabah Farouk - Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt
Ahmed Abd El Maksoud - Industrial Biotechnology Department, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt
Adel Guirgis - Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt
Hany Khalil - Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt

Background: Colorectal cancer (CRC), caused by abnormal cells growing in the colon or rectum, has a high mortality rate worldwide. On the other hand, microRNAs are small non-coding RNAs that contain approximately ۲۲ nucleotides in length. They are upregulated in a wide range of human cancers such as CRC. MiRNA-۲۱ post-transcriptionally regulates the expression of many tumor suppressor genes such as P۵۳ gene. This indicates that miRNA-۲۱ interacts like oncogenes and is required for CRC development. Method: The current original study was conducted in the National Liver Institute, Menofyia University, Egypt. We collected a total of ۴۰ blood samples from CRC patients ۴۰ samples from healthy individuals who served as controls. Quantitative real-time PCR detected the levels of miRNA-۲۱ and the fold changes of phosphates-tensin homology (PTEN) gene expression, as a tumor suppressor gene, in blood samples. Results: The expression levels of miR-۲۱ were upregulated in all obtained samples from patients with CRC in association with aging, gender, and tumor-node-metastasis staging. Furthermore, patients with poor and well-differentiated CRC revealed reduced levels of PTEN gene expression. We observed a putative binding site of miR-۲۱ in PTEN gene sequences. This indicates the direct cleavage between miR-۲۱ and PTEN coding sequence. Prediction analysis for other potential targets identified several malignancy factors and tumor suppressor genes with putative seeding regions for miR-۲۱ such as STAT۳, transforming growth factor-beta, tumor necrosis factor-α (TNF-α), and programmed cell death CD۴. Conclusion: The current data exhibited the potential dual role of hsa-miR-۲۱ in regulating cancer progression and showed that hsa-miR-۲۱ is an efficacious biomarker for CRC d evelopment and an attractive candidate for CRC treatment during early transformation.

Colorectal cancer, hsa-miR-۲۱, Dual response