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Islet Co-Expression of CD133 and ABCB5 in Human Retinoblastoma Specimens
Marco Zschoche1, Sergej Skosyrski2, Neele Babst1
1Department of Ophthalmology, University of Lübeck, Lübeck, Germany.
Background:
The role of CD133 und ABCB5 is discussed in treatment resistance in several types of cancer. The objective of this study was to evaluate whether CD133+/ABCB5+ colocalization differs in untreated, in beam radiation treated, and in chemotherapy treated retinoblastoma specimens. Additionally, CD133, ABCB5, sphingosine kinase 1, and sphingosine kinase 2 gene expression was analyzed in WERI-RB1 (WERI RB1) and etoposide-resistant WERI RB1 subclones (WERI ETOR).
Methods:
Active human untreated retinoblastoma specimens (n = 12), active human retinoblastoma specimens pretreated with beam radiation before enucleation (n = 8), and active human retinoblastoma specimens pretreated with chemotherapy before enucleation (n = 7) were investigated for localization and expression of CD133 and ABCB5 by immunohistochemistry. Only specimens with IIRC D, but not E, were included in this study. Furthermore, WERI RB1 and WERI ETOR cell lines were analyzed for CD133, ABCB5, sphingosine kinase 1, and sphingosine kinase 2 by the real-time polymerase chain reaction (RT-PCR).
Results:
Immunohistochemical analysis revealed the same amount of CD133+/ABCB5+ colocalization islets in untreated and treated human retinoblastoma specimens. Quantitative RT-PCR analysis showed a statistically significant upregulation of CD133 in WERI ETOR (p = 0.002). No ABCB5 expression was detected in WERI RB1 and WERI ETOR. On the other hand, SPHK1 (p = 0.0027) and SPHK2 (p = 0.017) showed significant downregulation in WERI ETOR compared to WERI RB1.
Conclusions:
CD133+/ABCB5+ co-localization islets were noted in untreated and treated human retinoblastoma specimens. Therefore, we assume that CD133+/ABCB5+ islets might play a role in retinoblastoma genesis, but not in retinoblastoma treatment resistance.
Insights
CD133 and ABCB5 colocalization islets are present in retinoblastoma, regardless of treatment. These CD133+/ABCB5+ islets may contribute to retinoblastoma development but not treatment resistance.
Area of Science:
- Oncology
- Cancer Biology
- Retinoblastoma Research
Background:
- CD133 and ABCB5 are implicated in cancer treatment resistance.
- Their role in retinoblastoma treatment resistance requires further investigation.
Purpose of the Study:
- To compare CD133+/ABCB5+ colocalization in untreated, radiation-treated, and chemotherapy-treated retinoblastoma.
- To analyze gene expression of CD133, ABCB5, sphingosine kinase 1 (SPHK1), and sphingosine kinase 2 (SPHK2) in retinoblastoma cell lines.
Main Methods:
- Immunohistochemistry was used to assess CD133 and ABCB5 localization in human retinoblastoma specimens.
- Real-time PCR analyzed gene expression in WERI-RB1 and etoposide-resistant WERI RB1 (WERI ETOR) cell lines.
Main Results:
- CD133+/ABCB5+ colocalization islets were observed in both untreated and treated retinoblastoma specimens.
- CD133 showed significant upregulation in WERI ETOR cells, while ABCB5 expression was not detected.
- SPHK1 and SPHK2 were significantly downregulated in WERI ETOR cells.
Conclusions:
- CD133+/ABCB5+ islets are present in retinoblastoma, suggesting a role in tumor genesis.
- These findings indicate that CD133+/ABCB5+ islets are not associated with retinoblastoma treatment resistance.
