miR-27b-3p a Negative Regulator of DSB-DNA Repair

Abstract

Understanding the regulation of DNA repair mechanisms is of utmost importance to identify altered cellular processes that lead to diseases such as cancer through genomic instability. In this sense, miRNAs have shown a crucial role. Specifically, miR-27b-3 biogenesis has been shown to be induced in response to DNA damage, suggesting that this microRNA has a role in DNA repair. In this work, we show that the overexpression of miR-27b-3p reduces the ability of cells to repair DNA lesions, mainly double-stranded breaks (DSB), and causes the deregulation of genes involved in homologous recombination repair (HRR), base excision repair (BER), and the cell cycle. DNA damage was induced in BALB/c-3T3 cells, which overexpress miR-27b-3p, using xenobiotic agents with specific mechanisms of action that challenge different repair mechanisms to determine their reparative capacity. In addition, we evaluated the expression of 84 DNA damage signaling and repair genes and performed pathway enrichment analysis to identify altered cellular processes. Taken together, our results indicate that miR-27b-3p acts as a negative regulator of DNA repair when overexpressed.

Circ_0001671 regulates prostate cancer progression through miR-27b-3p/BLM axis

“…MiRNA is predominantly implicated in the suppression of mRNA expression by targeting the 3' UTR of specific genes. One such miRNA, MiR-27b-3p, has been identified as a potential tumor suppressor across various cancer types 33 . Investigations have demonstrated that MiR-27b-3p exerts a negative regulatory effect on DNA repair and exhibits diminished expression in lung cancer tissues 34 .…”

Human Adult Renal Progenitor Cells Prevent Cisplatin-Nephrotoxicity by Inducing CYP1B1 Overexpression and miR-27b-3p Down-Regulation through Extracellular Vesicles

“…In this study, we investigated the presence of a particular miRNA, miR-27b-3p, which is responsible for the regulation of CYP1B1 [ 19 , 37 , 38 , 39 , 40 ] and is involved in renal diseases [ 41 ]. In breast cancerous tissues miR-27b-3p level is decreased compared to non-cancerous tissues, leading to the high expression of CYP1B1 [ 42 , 43 ].…”

“…At renal level, the CYP1B1 overexpression induced in RPTEC by tARPC can be interpreted as an attempt to protect RPTEC from cisplatin-induced nephrotoxicity and may open an important strategy of prevention of AKI before starting chemotherapy. In this study, we investigated the presence of a particular miRNA, miR-27b-3p, which is responsible for the regulation of CYP1B1 [19,[37][38][39][40] and is involved in renal diseases [41]. In breast cancerous tissues miR-27b-3p level is decreased compared to non-cancerous tissues, leading to the high expression of CYP1B1 [42,43].…”