Hsa-miR-21-mediated Cell Death and Tumor Metastases: A Potential Dual Response During Colorectal Cancer Development

Background: Colorectal cancer (CRC), caused by abnormal cells growing in the colon or the rectum, has a high mortality rate worldwide. On the other hand, microRNAs are small noncoding RNAs that contain approximately 22 nucleotides in length. They are up-regulated in a wide range of human cancers such as CRC. MiRNA-21 post-transcriptionally regulates the expression of many tumor suppressor genes such as P53 gene. This indicates that miRNA-21 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 40 blood samples from CRC patients 40 samples from healthy individuals who served as controls. Quantitative real-time PCR detected the levels of miRNA-21 and the fold changes of phosphates-tensin homology (PTEN) gene expression, as a tumor suppressor gene, in blood samples. Result: The expression levels of miR-21 were up-regulated 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-21 in PTEN gene sequences. This indicates the direct cleavage between miR-21 and PTEN coding sequence. Prediction analysis for other potential targets identified several malignancy factors and tumor suppressor genes with putative seeding regions for miR-21 such as STAT3, transforming growth factor-beta, tumor necrosis factor-α (TNF-α), and programmed cell death CD4. Conclusion: The current data exhibited the potential dual role of hsa-miR-21 in regulating cancer progression and showed that hsa-miR-21 is an efficacious biomarker for CRC development and an attractive candidate for CRC treatment during early transformation.