Find in Library

miR-29b2 and miR-29c play a suppressive role in breast cancer progression. <i>C1orf132</i> (also named <i>MIR29B2CHG</i>) is the host gene for generating both microRNAs. However, the region also expresses longer transcripts with unknown functions. We employed bioinformatics and experimental approaches to decipher <i>C1orf132</i> expression and function in breast cancer tissues. We also used the CRISPR/Cas9 technique to excise a predicted <i>C1orf132</i> distal promoter and followed the behavior of the edited cells by real-time PCR, flow cytometry, migration assay, and RNA-seq techniques. We observed that <i>C1orf132</i> long transcript is significantly downregulated in triple-negative breast cancer. We also identified a promoter for the longer transcripts of <i>C1orf132</i> whose functionality was demonstrated by transfecting MCF7 cells with a <i>C1orf132</i> promoter-GFP construct. Knocking-out the promoter by means of CRISPR/Cas9 revealed no alterations in the expression of the neighboring genes <i>CD46</i> and <i>CD34</i>, while the expression of miR-29c was reduced by half. Furthermore, the promoter knockout elevated the migration ability of the edited cells. RNA sequencing revealed many up- and downregulated genes involved in various cellular pathways, including epithelial to mesenchymal transition and mammary gland development pathways. Altogether, we are reporting here the existence of an additional/distal promoter with an enhancer effect on miR-29 generation and an inhibitory effect on cell migration.