SPI1 Promotes TNF-α-Induced Epithelial-Mesenchymal Transition-Like Changes in Retinal Pigment Epithelial Cells: Implications for the Pathogenesis of Age-Related Macular Degeneration.

Authors

Xingyi Zhang, Hua Liu

Published in

Journal of ophthalmology. Volume 2026. Pages 8106992. Epub Jul 29, 2026.

Abstract

Age-related macular degeneration (AMD) is a progressive degenerative disease of the retinal macula associated with aging, which is one of the main causes of vision loss in the elderly. This research aims to investigate the mechanism of SPI1 in EMT of RPE cells in AMD, providing new targets for AMD treatment.
SPI1, ALKBH5, and NURR1 expression was assayed by RT-qPCR and Western blot in AMD patients and cell models. The relationship between SPI1 expression and clinical features of AMD patients was analyzed, and the correlations among SPI1, ALKBH5, and NURR1 were analyzed. The diagnostic value of SPI1 in AMD was verified via ROC curve. ROS levels were detected. N-cadherin and E-cadherin were detected by Western blot. Cell migration was detected by transwell assay. The binding of SPI1 to ALKBH5 in cells was verified. m6A levels on NURR1 were detected.
SPI1 and ALKBH5 were highly expressed, while NURR1 was lowly expressed in TNF-α-induced human RPE cells. SPI1 expression was correlated with age and staging of AMD patients. SPI1 expression exhibited a positive association with ALKBH5 expression, while showing a negative association with NURR1 expression. After downregulation of SPI1, N-cadherin was downregulated, E-cadherin was upregulated, ROS levels were decreased, and cell migration was reduced. SPI1 promoted ALKBH5 expression, and ALKBH5 downregulated NURR1 expression via m6A modification. ALKBH5 overexpression or NURR1 downregulation partially reversed the attenuating effect of SPI1 downregulation on EMT-like changes in RPE cells.
SPI1 stimulates EMT-like changes of RPE cells via the ALKBH5/NURR1 axis. This pathway may participate in AMD-related pathological processes.

PMID:
42534447
Bibliographic data and abstract were imported from PubMed on 31 Jul 2026.

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