AI Article Synopsis
- Retinoblastoma (RB) is the most common eye cancer in children and is linked to mutations in a specific tumor suppressor gene.
- Previous research identified this gene as a novel tumor suppressor involved in the regulation of epithelial-mesenchymal transition (EMT) and found its location significant for RB malignancy onset.
- The study revealed that the gene plays a role in RB progression by affecting the cancer microenvironment, and its loss leads to decreased cell adhesion and increased EMT, suggesting it could be a potential target for new RB treatments.
Article Abstract
Retinoblastoma (RB) is the most common intraocular pediatric cancer. Nearly all cases of RB are associated with mutations compromising the function of the tumor suppressor gene. We previously demonstrated that is widely downregulated in various cancers and our in vivo and in vitro analysis revealed as a novel tumor suppressor and regulator of EMT. In addition, 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 in RB through in vitro analysis and next-generation sequencing. Immunostaining revealed that is expressed in Müller glial cells in the retina. mRNA expression profiling of mouse retina and -treated RB cells found that contributes to RB progression via regulation of the cancer microenvironment, in which loss of reduces cell-cell adhesion and facilitates EMT. Our observations suggest that may have potential as a new strategy for RB treatment.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9563430 | PMC |
| http://dx.doi.org/10.3390/cancers14194926 | DOI Listing |
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