Relation between the circular and linear form of the Elongator Acetyltransferase Complex Subunit 3 in the progression of triple‐negative breast cancer

Triple‐negative breast cancer (TNBC) is the most aggressive type of breast cancer (BC) that hardly responds to common treatment. Recent studies show that circ‐ELP3 (Elongator Acetyltransferase Complex Subunit 3 or hsa‐circ‐0001785) is involved in the pathogenesis of several malignancies. The present study aimed to evaluate the possible role of this circRNA in the progression of TNBC cells and the possible relation between the circular and linear forms of the ELP3. We evaluated the circ‐ELP3 and its host gene expression level in clinical samples and breast cancer cell lines. Using an expression vector, hsa‐circ‐0001785 was upregulated to investigate its role on cancer cell progression. After a transient transfection, we evaluated possible alterations in the cell cycle progression, cell viability, and cell proliferation. Quantitative real‐time polymerase chain reaction analyses verified that circ‐ELP3 and its host gene were significantly upregulated in TNBC tissues and breast cancer cells. Overexpression of circ‐ELP3 markedly increases the cell viability and proliferation and also the formation of colonies in transfected cells compared to the controls. Briefly, our results showed that Circ‐ELP3 and its host gene were significantly upregulated in TNBC. Circ‐ELP3 is involved in TNBC progression and may exert its effects by indirectly regulating of ELP3 expression. Significance statement Nowadays, more research is focused on the role of circular RNAs in diagnosis, treatment, and prevention of breast cancer to reduce its mortality. Accordingly, previous studies have shown an oncogenic role for circ‐ELP3 (hsa‐circ‐0001785) in breast cancer progression. There is no evidence of the relation between the circular and linear form of the Elongator Acetyltransferase Complex Subunit 3 (ELP3) gene. Expression level of circ‐ELP3 in breast cancer samples was significantly upregulated compared to normal tissues, at the same time ELP3 was markedly increased in samples. Overexpression of circ‐ELP3 promoted the viability and proliferation of breast cancer cells, particularly triple‐negative breast cancer (TNBC) cell lines. It was first displayed in our study that the expression level of the circ‐ELP3 is directly correlated with the expression of ELP3, its host gene. The overexpression of ELP3 through circ‐ELP3 can enhance the breast cancer cell proliferation, which provided us a novel molecular mechanism in TNBC.