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 rectum, has a high mortality rate worldwide. on the other hand, micrornas are small non-coding rnas that contain approximately 22 nucleotides in length. they are upregulated 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.results: the expression levels of mir-21 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-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.