PIWI interacting RNAs (piRNAs), a member of non-coding RNA, originate from intergenic repetitive regions of the genome. piRNA expressions increase in various cancers and it is thought that this increase could be caused by hormones. We aimed to determine the effects of hormones on piRNA expression in breast and prostate cancer. High viability and a decrease in adhesion were observed at the concentrations of the highest proliferation. Furthermore, an increase in adhesion was also observed in MDA-MB-231 cells. After hormone treatment, while piR-651 expression had increased both breast and prostate cancer cell lines, piR-823 expressions increased in prostate cancer cell lines and only in the breast cancer cell line which was malignant. Thus, it was determined that piR-823 might show different expressions in different type of cancers.

Micro RNA-126 coordinates cell behavior and signaling cascades according to characteristics of breast cancer cells

PIWI-Interacting RNAs are small non-coding RNAs derived from single-stranded RNAs which plays a crucial role in epigenetic regulation through transposon silencing and mRNA degradation via deamination. This study aimed to inhibit piR-651 and piR-823 in MDA-MB-231 triple-negative breast cancer cells and to explore their potential effects on healthy HUVEC cells. Non-target, anti-piR-651, and anti-piR-823 sequences were transfected in bothHUVEC and MDA-MB-231 cells using Lipofectamine. Proliferation and motility were assessed at 24, 48, and 72 h post-transfection in both cell lines. Based on the motility findings, MDA-MB-231 cells were underwent an invasion assay using crystal violet staining. The expressions of Ki-67, HIF-1α, MMP-2, and MMP-9 genes were measured at 48 h, when both cell lines exhibited the most significant effects of inhibition. The optimal time for proliferation of anti-piR-651 and anti-piR-823 transfected MDA-MB-231 cells was determined to be at 48 h, as indicated by decreased motility and invasion assay results (p < 0.001). NeverthelessHowever, there was no significant difference in the motility and proliferation of HUVECss transfected with anti-piR-651 and anti-piR-823 compared to the control group (p > 0.05). Asides from MMP-2 in anti-piR-823 transfected HUVECs and HIF-1α in anti-piR-823 transfected MDA-MB-231 cells, gene expressions of Ki-67, HIF-1α, MMP-2, and MMP-9 were reduced in both cell lines (p < 0.001). Inhibition of piR-651 and piR-823 decreased the survival and metastasis of cancer cells, without causing vital structural changes in healthy cells. Future research in cancer gene therapy or genetic modification may benefit from investigating piR-651 and piR-823 as possible inhibitors of breast cancer invasion and metastasis.

Capsaicin is a natural product which is extracted from pepper and has the potential to be used in cancer treatment because of its anti- proliferative effects. The aim of the study was to determine the effect of capsaicin on the hepatocellular carcinoma cell proliferation and the expressions of related genetic markers as Ki-67, PI3K/AKT/mTOR and epigenetic markers as miR-126 and piR-Hep-1. The inhibitory concentration of capsaicin in HepG2 cells was determined. piR-Hep-1 and miR-126 expressions and Ki-67, PI3K, AKT and mTOR gene expressions were examined by RT-PCR. The inhibitory concentration of capsaicin for HepG2 cells was 200 nM and the decreased proliferation was observed at 24th hour. As epigenetic markers, an up regulation of miR-126 and down regulation of piR-Hep-1 expression were determined after treatment. Moreover, Ki-67, PI3K and mTOR gene expressions decreased while AKT gene expression increased after the treatment (p<0.001). According to the obtained data, capsaicin has an impact on proliferation both genetically and epigenetically. Furthermore, treatment of capsaicin effects miR-126 and piR-Hep-1 expressions which effect carcinogenesis in different way. Moreover, there are some clues which indicate that these two small non-coding RNA might affect each other and share the same target molecules post-transcriptionally.

Objectives: Triple negative breast cancer cells are estrogen, progesterone, and HER receptor negative, malign breast cancer cells. These cells have high telomerase activity, and this activity gives these cells high proliferation and evading apoptosis abilities. In this study, we aimed to determine the affect piR-823 on genetic parameters of proliferation and ERα status in MDA-MB-231 cells. Methods: After anti-piR-823 transfection, proliferation of cells was tested by XTT. Gene expressions were determined by RT-PCR. Protein expressions were determined by ELISA. Results: The proliferation decreased after inhibition (p<0.001). Gene and protein expressions of ERα were upregulated while hTERT was downregulated after inhibition (p<0.001). Furthermore, piR-823 inhibition cause to decrease PI3K/ AKT/mTOR gene expressions and miR-126 expression (p<0.001). Conclusion: Obtained data indicates that piR-823 inhibition lead MDA-MB-231 cells to increase ERα expression. Decreased expressions of hTERT and PI3K/AKT/mTOR pathway affect cell proliferation. Moreover, miR-126 decrease indicates that piRNAs and miRNAs can share the same target molecules and piRNA expression changes might have an impact on miRNA expressions. All obtained data is important on the perspective of piRNAs and their effect on cellular characteristics of triple negative breast cancer cells.

4-Hydroxycoumarin is an aromatic substance which is metabolized in liver and used as a therapeutic agent for various diseases. We aimed to determine the im