Omentin-1 is associated with the expression of proliferation, migration, and PI3K/AKT-related genes in breast cancer cells

Background: Breast cancer (BC) progression is regulated not only by intrinsic tumor characteristics but also by the tumor microenvironment, including adipose tissue-derived adipokines.Omentin-1 (intelectin-1) is a visceral adipokine implicated in metabolic regulation and inflammation; however, its role in BC remains controversial and insufficiently defined.Aims: This study aimed to evaluate the effects of omentin-1 on the proliferation, adhesion, and migration of BC cells and to investigate its association with the expression of PIK3CA/AKT1-related and migration-associated genes.Methods: MCF-7 (estrogen receptor-positive, weakly invasive) and MDA-MB-231 (estrogen receptor-negative, highly invasive) BC cell lines were treated with 100 and 200 ng/mL of recombinant omentin-1 for 24 and 48 h.Cell proliferation was assessed using the XTT assay, adhesion by an XTT-based method after washing, and migration via a wound-healing assay.The expression levels of PIK3CA, AKT1, and MMP-9 were analyzed by quantitative real-time polymerase chain reaction.Statistical significance was set at p < 0.05. Results:Omentin-1 significantly reduced proliferation in MCF-7 cells at 48 h by 20%-30% relative to control (p < 0.001), whereas no significant effect was observed in MDA-MB-231 cells (p > 0.05).Adhesion remained unchanged in the two cell lines (94%-100% across all groups, p > 0.05).Migration was significantly inhibited in MCF-7 cells at 72 h, with gap closure declining from 85.71% to 62.98% and 58.98% (p = 0.031; p = 0.001).In contrast, MDA-MB-231 cells responded in a limited, time-dependent manner, with enhanced migration at 24 h and with no variations at 72 h due to complete closure.Gene expression analysis revealed dose-and time-dependent changes in transcription of PIK3CA, AKT1, and MMP-9, with each cell line showing distinct patterns. ÖzetDayanak: Meme kanseri progresyonu, yalnızca tümöre özgü intrinsik özellikler tarafından değil, aynı zamanda adipoz dokudan kaynaklanan adipokinleri de içeren tümör mikroçevresi tarafından düzenlenmektedir.Omentin-1 (intelectin-1), metabolik düzenleme ve inflamasyon süreçlerinde rol oynadığı bilinen visseral kökenli bir adipokindir; ancak meme kanserindeki rolü hâlen