PRELP regulates cell–cell adhesion and EMT and inhibits retinoblastoma progression

Jack Hopkins, Ken Asada, Alex Leung, Vasiliki Papadaki, Hongorzul Davaapil, Matthew Morrison, Tomoko Orita, Ryohei Sekido, Hirofumi Kosuge, M. Ashwin Reddy, Kazuhiro Kimura, Akihisa Mitani, Kouhei Tsumoto, Ryuji Hamamoto, Mandeep S. Sagoo, Shin Ichi Ohnuma*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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Retinoblastoma (RB) is the most common intraocular pediatric cancer. Nearly all cases of RB are associated with mutations compromising the function of the RB1 tumor suppressor gene. We previously demonstrated that PRELP is widely downregulated in various cancers and our in vivo and in vitro analysis revealed PRELP as a novel tumor suppressor and regulator of EMT. In addition, PRELP is located at chromosome 1q31.1, around a region hypothesized to be associated with the initiation of malignancy in RB. Therefore, in this study, we investigated the role of PRELP in RB through in vitro analysis and next-generation sequencing. Immunostaining revealed that PRELP is expressed in Müller glial cells in the retina. mRNA expression profiling of PRELP−/− mouse retina and PRELP-treated RB cells found that PRELP contributes to RB progression via regulation of the cancer microenvironment, in which loss of PRELP reduces cell–cell adhesion and facilitates EMT. Our observations suggest that PRELP may have potential as a new strategy for RB treatment.

Original languageEnglish
Article number4926
Number of pages22
Issue number19
Publication statusPublished - 8 Oct 2022


  • cell–cell adhesion
  • dysplasia
  • retinoblastoma
  • UKRI
  • MRC
  • MR/K501268/1


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