Turgut Coşan, DidemSoyocak, AhuÖner, Çağrı2024-07-122024-07-122018Turgut Coşan, D., Soyocak, A. ve Öner, Ç. (2018). The silenced potassium channels Kv1.3 and Kv10.1 affects miR-126 in breast cancer cells. Abstracts from the 50th European Society of Human Genetics Conference: Posters, Nature. s. 574.https://www.nature.com/articles/s41431-018-0247-7https://hdl.handle.net/20.500.12415/3324Introduction: It has been shown that non-coding regulatory RNAs, especially play a role in formation and progression of cancer. miR-126 is markedly downregulated in human breast cancer tissues. Various studies indicate that some voltage gated potassium channels are also overexpressed in the tumor. Kv1.3, a member of the voltage-gated potassium channel family is overexpressed in cancerous breast tissues than in normal breast tissues. Another protein, Kv10.1 is overexpressed in many human tumors, including breast cancer and it has oncogenic properties. Ether à go-go 1 (Eag1) channel is overexpressed in a variety of cancers and plays important roles in cancer progression. However, the association between with voltage gated potassium channels and miR-126 is unclear. In our study, we aimed to show whether there is association between miR-126/miR-126* and Kv1.3 or Kv10.1 in non-invasive estrogen positive MCF-7 and invasive estrogen negative MDA-MB-231 human BC cells. Materials and Methods: MCF-7 and MDA-MB-231 cells were transfected with Kv1.3 and Kv10.1 specific siRNA. miR-126 and miR-126* expression was determined in total RNA isolated from the cells. All samples were normalized to the internal controls, and fold changes were calculated through relative quantification (2???Ct). Results: The results of our research indicate that there is a strong inverse relationship with the expression levels of miR-126 and potassium channels. Conclusions: The miR-126/126* expressions increased in the MDA-MB-231 cells and decreased in the MCF-7 cells by using siRNA against potassium channels Kv1.3 and Kv10.1.eninfo:eu-repo/semantics/openAccessConference Object574