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February 26, 2026Discovery Medicine0 citations

Function and Mechanism of SLC38A5 in Retinoblastoma Development

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CWChao WuYDYan DengXXXiaoyan Xiong

Key Points

  • To investigate the expression and role of SLC38A5 in retinoblastoma development.
  • Analyzed SLC38A5 expression in RB cell lines using Western blotting and qRT-PCR.
  • Performed genetic manipulation (knockdown/overexpression) for functional characterization.
  • Evaluated tumor growth using in vivo xenograft models.
  • SLC38A5 was overexpressed in RB cell lines, notably Y79 and WERI-Rb1 (<p < 0.001).
  • SLC38A5 knockdown reduced cell proliferation, migration, and invasion, inducing apoptosis (<p < 0.05).
  • Overexpression of SLC38A5 enhanced malignant phenotypes (<p < 0.05).
  • SLC38A5 influenced mitochondrial function through the mTOR signaling pathway (<p < 0.05).
  • In vivo, SLC38A5 overexpression promoted tumor growth, while knockdown inhibited progression (<p < 0.05).

Abstract

Background: Retinoblastoma (RB) is a highly aggressive pediatric ocular malignancy whose molecular mechanisms remain unclear. Although implicated in various cancers, the amino acid transporter Solute Carrier Family 38 Member 5 (SLC38A5) remains uncharacterized in RB. Herein, we aimed to investigate the expression pattern, biological functions, and underlying mechanisms of SLC38A5 in RB. Methods: SLC38A5 expression was analyzed in human RB cell lines using Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). Functional characterization was performed through genetic manipulation (knockdown/overexpression) followed by comprehensive phenotypic assessment. In vivo xenograft models were used to evaluate tumor growth. Results: SLC38A5 was significantly overexpressed in RB cell lines, particularly in Y79 and WERI-Rb1 (p p p p In vivo, SLC38A5 overexpression promoted tumor growth, whereas knockdown inhibited tumor progression (p < 0.05). Conclusion: SLC38A5 acts as a key regulator of RB progression by modulating core biological processes, including proliferation, migration, invasion, and mitochondrial function. Targeting SLC38A5 may represent a potential therapeutic strategy for RB.

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Cite This Study

Wu et al. (2026) studied this question.

synapsesocial.com/papers/699f95951bc9fecf3dab3850https://doi.org/10.24976/discov.med.202638205.41
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