Open Access

ARTICLE

PIWI Interacting RNA-651 Inhibition Transforms the Genetic Features of MCF-7 Breast Cancer Cells

Çağrı Öner^1,* and Ertuğrul Çolak²

¹ Medical Faculty, Department of Medical Biology and Genetics, Maltepe University, İstanbul, 34857, Turkey
² Medical Faculty, Departfiment of Biostatistics, Eskişehir Osmangazi University, Eskişehir, 26040, Turkey
^* Corresponding Author: Çağrı Öner. Email: cagri.oner@maltepe.edu.tr

Oncologie 2021, 23(3), 393-407. https://doi.org/10.32604/Oncologie.2021.016958

Received 14 April 2021; Accepted 22 June 2021; Issue published 26 September 2021

Abstract

piRNAs are novel members of small non-coding RNAs and have an impact on genetic and epigenetic mechanisms of cells. It was aimed to investigate the role of piR-651 on MCF-7 benign breast cancer cells by focusing on molecular characteristics. Anti-piR-651 was transfected and effects of piR-651 on proliferation, adhesion, and motility of MCF-7 cells were detected after the 24th, 48th, and 72nd hour. Gene expressions of piR-651, Ki-67, MMP-2, ERα, HIF-1α, and hTERT were determined by using RT-PCR. piR-651 inhibition caused the decrease of proliferation, adhesion (p < 0.001), and motility of MCF-7 cells. The efficiency of anti-piR-651 transfection supported the determination of the decrease of piR-651 expression after transfection after the 48th hour (p < 0.001). AntipiR-651 transfection caused the downregulation of Ki-67, MMP-2, ERα, HIF-1α, and hTERT gene expressions after the 48th hour (p < 0.001). In MCF-7 cells, piR-651 inhibition can change both cellular characteristics and gene expressions which were related to these characteristics. piR-651 inhibition causes the decrease of both proliferation and adhesion of cells, which are especially important cellular marks of MCF-7 cells. These results have shed light on whether we can mitigate the effects of cancer cells via piRNA inhibition. The absence of piRNA expression caused the change of fate of benign breast cancer cells by decreasing malign features of MCF-7 cells.

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