Expression of CircATXN7 in esophageal cancer tissues and its effect on cell proliferation and invasion.

Background: The goal of the current research was to investigate circATXN7 expression in esophageal cancer (EC) and its impact on the proliferation, migration, and invasion of EC cells.

Methods: Determination of circATXN7 expression in esophageal cancer tissues and adjacent tissueswas carried out using quantitative reverse transcription polymerase chain reaction (qRT-PCR), and we further analyzed the correlation between patients' clinical characteristics and circATXN7 expression. EC cell lines (EC-9706, Eca-109, TE-1, KYSE-30, and KYSE-150) and normal esophageal cell line (HET-1A) were cultured, and circATXN7 expression was detected by qRT-PCR. The lowest circATXN7-containing Eca-109 cells were selected to be transfected with an overexpressing lentiviral vector (circATXN7). EC-9706 cells with the highest expression of circATXN7 were selected for transfection with knockdown vectors [short hairpin RNA (shRNA)#1 and shRNA#2] of the circATXN7 sequence. Cell proliferation was determined via MTT assay. The formation of cell clones was investigated via colony formation assay. Transwell migration assay was utilized to determine cell migration and invasion ability.

Results: Significantly higher levels of circATXN7 were observed in EC tissues compared with paracancerous tissues (P<0.01), and circATXN7 expression level showed a significant correlation with the tumor/lymph nodes/metastasis (TNM) stage and metastasis of lymph nodes (P<0.05). Among all esophageal cell lines, EC-9706 had the highest expression level and Eca-109 had the lowest expression level. The MTT assay revealed that circATXN7 overexpression could significantly promote the proliferation of Eca-109 cells, while circATXN7 knockdown was capable of significantly inhibiting EC cell proliferation. The colony formation experiments revealed a significant increase in the number of clones in the circATXN7 overexpression model and a significant decrease in the circATXN7 knockdown model. The results of transwell migration experiments suggested that circATXN7 overexpression could promote EC cell invasion and migration, while knockdown of circATXN7 expression was associated with significant inhibition of the invasion and migration of these cells.

Conclusions: CircATXN7 exerted a critical role in the incidence and progression of EC. This study identified a novel molecular target and established a theoretical basis for the early detection and treatment of EC.