Iranian
Biomedical Journal
Volume 29, Issue 6 (11-2025)
IBJ 2025, 29(6): 397-404 |
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Köstü S, Bakirci B, Şimşek E B, Dumanli D, Çelik A, Kaya A, et al . Transcriptional Control of PI3K/AKT/mTOR by piRNA-651 in Breast Carcinoma. IBJ 2025; 29 (6) :397-404
URL: http://ibj.pasteur.ac.ir/article-1-5229-en.html
URL: http://ibj.pasteur.ac.ir/article-1-5229-en.html
Sena Köstü 
, Baturalp Bakirci , Ece Bilge Şimşek , Defne Dumanli , Ahmetcan Çelik , Alara Kaya , Damla Kolcuoğlu , Ertuğrul Çolak , Çağrı Öner *
, Baturalp Bakirci , Ece Bilge Şimşek , Defne Dumanli , Ahmetcan Çelik , Alara Kaya , Damla Kolcuoğlu , Ertuğrul Çolak , Çağrı Öner *
Abstract:
Background: Breast cancer is among the most prevalent malignancies in women worldwide, yet early diagnosis is associated with a high survival rate. The proliferation of BC is linked to the overexpression of genes within the PI3K/AKT/mTOR signaling pathway. piR-651 has been reported to be effective in the proliferation and metastasis of BC. This research sought to evaluate the impact of piR-651 inhibition on the PI3K/AKT/mTOR pathway in HUVEC, MCF-7, and MDA-MB-231 cells.
Methods: Anti-piR-651 and non-target sequences were introduced into HUVEC, MCF-7, and MDA-MB-231 BC cells by lipofectamine transfection. After 48 hours, total RNA was extracted, and qRT-PCR assessed the gene expression of PI3K, AKT, and mTOR.
Results: Anti-piR-651 treatment significantly increased PI3K, AKT, and mTOR gene expression in HUVECs (p < 0.001). In contrast, PI3K and mTOR expression decreased in MCF-7 and MDA-MB-231 cells (p < 0.001), while AKT expression remained unchanged in MDA-MB-231 cells (p > 0.05). Correlations between these genes varied by cell type, with significant associations observed at p < 0.05 or p < 0.01, depending on the group.
Conclusion: piR-651 inhibition causes AKT to behave independently of PI3K and mTOR, particularly in MCF-7 cells, suggesting limited gene therapy potential for estrogen receptor-positive BC. Preliminary data indicate that piR-651 inhibition may reduce BC cell proliferation through effects on PI3K and mTOR.
Methods: Anti-piR-651 and non-target sequences were introduced into HUVEC, MCF-7, and MDA-MB-231 BC cells by lipofectamine transfection. After 48 hours, total RNA was extracted, and qRT-PCR assessed the gene expression of PI3K, AKT, and mTOR.
Results: Anti-piR-651 treatment significantly increased PI3K, AKT, and mTOR gene expression in HUVECs (p < 0.001). In contrast, PI3K and mTOR expression decreased in MCF-7 and MDA-MB-231 cells (p < 0.001), while AKT expression remained unchanged in MDA-MB-231 cells (p > 0.05). Correlations between these genes varied by cell type, with significant associations observed at p < 0.05 or p < 0.01, depending on the group.
Conclusion: piR-651 inhibition causes AKT to behave independently of PI3K and mTOR, particularly in MCF-7 cells, suggesting limited gene therapy potential for estrogen receptor-positive BC. Preliminary data indicate that piR-651 inhibition may reduce BC cell proliferation through effects on PI3K and mTOR.
Type of Study: Full Length/Original Article |
Subject:
Cancer Biology
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