investigating mir-16-5p: the tumor suppressor that influences cell cycle genes in colorectal cancer

Background: colorectal cancer (crc) remains a major health challenge, with perturbation in the cell cycle playing a crucial role in its progression. hsa-mir-16-5p (mir-16-5p) is a crucial tumor suppressor, but its precise role in modulating cell cycle genes, particularly in the presence of ionizing radiation, is not fully understood.objective: this study investigated the role of mir-16-5p in modulating the expression of cell cycle genes in colorectal cancer cells exposed to ionizing radiation.material and methods: in this experimental study, ht-29 cells were transfected with mir-16-5p using the polyfectamine transfection reagent. expression levels of mir-16-5p, cyclin-dependent kinase 4 (cdk4), cyclin e1 (ccne1), and cyclin d1 (ccnd1) were quantified by real-time polymerase chain reaction (pcr). to assess the changes after irradiation, cells were exposed to 4 gy.results: ionizing radiation significantly downregulated mir-16-5p compared to controls, while transfection of mir-16-5p significantly increased its expression level. however, irradiation of 4 gy did not significantly alter ccnd1 or ccne1, but decreased cdk4 expression. the mir-16-5p transfection significantly suppressed ccnd1, ccne1 and cdk4 compared to controls. the expression of ccnd1, ccne1, and cdk4 significantly decreased when mir-16-5p transfection was performed before 4 gy irradiation compared to both 4 gy irradiation alone and the control group. conclusion: our results highlight the role of mir-16-5p in modulating key cell cycle genes in crc. increasing mir-16-5p expression could improve radiosensitivity and represent a therapeutic strategy for the treatment of crc.