Circulating UCA1 is highly expressed in patients with systemic lupus erythematosus and promotes the progression through the AKT pathway

OBJECTIVE: To investigate the role of Urothelial Carcinoma Associated 1 (UCA1) during the progression of systemic lupus erythematosus (SLE) and the underlying mechanism.

PATIENTS AND METHODS: UCA1 expression in peripheral blood of SLE patients, as well as the expression of protein kinase B (AKT) in the peripheral blood mononuclear cell (PBMC), was detected by qRT-PCR. Expression differences in UCA1 and AKT between different groups were compared by t-test or univariate analysis. Through correlation analysis, the correlation between UCA1, AKT and clinical indicators of patients was analyzed. After overexpression and knockout of UCA1, the effect on phenotypes of BaF3 cell was examined. Finally, we analyzed the correlation between AKT and UCA1, and the effect on AKT pathway after overexpression and knockout of UCA1.

RESULTS: We found that plasma level of UCA1 and AKT was significantly enhanced in SLE patients. By analyzing the clinical data, a higher UCA1 level was observed in female patients than in males. In addition, UCA1 level in SLE patients with active stage and pathological lesions was higher than those in a stable stage without organ involvement. Correlation analysis showed that there was a positive correlation between UCA1 and C3, anti-ds-DNA, ESR and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Similarly, there was a positive correlation between AKT and C3, anti-ds-DNA, erythrocyte sedimentation rate (ESR) and SLEDAI, respectively. After overexpression and knockdown of UCA1, it was found that overexpression of UCA1 significantly enhanced cell proliferation, while the interference with UCA1 significantly inhibited cell proliferation. Western blot revealed increased expressions of PI3K and AKT after overexpressing UCA1, whereas knockdown of UCA1 led significantly decreased expressions of PI3K and AKT.

CONCLUSIONS: UCA1 expression was significantly increased in SLE, which promoted the progression of SLE by activating AKT pathway.

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