ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis
Van Meenen D, Doege A, Alefeld E, Haase A, Beier M, Kiefer T, Biewald E, Metz K, Dräger O, Busch MA, Dünker N (2022)
International Journal of Molecular Sciences 23(20): 12621.
Zeitschriftenaufsatz
| Veröffentlicht | Englisch
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Autor*in
Van Meenen, Dario;
Doege, Annika;
Alefeld, Emily;
Haase, Andre;
Beier, Manfred;
Kiefer, Tobias;
Biewald, Eva;
Metz, Klaus;
Dräger, OliverUniBi;
Busch, Maike Anna;
Dünker, Nicole
Abstract / Bemerkung
A disintegrin and metalloproteinase (ADAM) family proteins, acting as sheddases, are important factors in a number of pathologies, including cancer, and have been suggested as promising therapeutic targets. The study presented focuses on the involvement of ADAM10 and ADAM17 in retinoblastoma (RB), the most common malignant intraocular childhood tumor. A significant correlation between ADAM17 expression levels and RB laterality and RB staging was observed. Levels of ADAM10 or ADAM17 regulating miRNAs miR-145, -152, and -365 were significantly downregulated in RB cell lines, and reduced miR levels with simultaneously upregulated ADAM10 and ADAM17 expression were found in RB patients. The involvement of both ADAMs analyzed in ectodomain shedding of the neuronal cell adhesion molecule L1 (L1CAM), shown to induce pro-tumorigenic effects in RB, was confirmed. Lentiviral ADAM10 and ADAM17 single or ADAM10/17 double knockdown (KD) induced caspase-dependent apoptosis and reduced cell viability, proliferation, growth, and colony formation capacity of RB cells. Moreover, differential phosphorylation of the serine/threonine kinase AKT was observed following ADAM17 KD in RB cells. Chicken chorioallantoic membrane (CAM) assays revealed that ADAM17 and ADAM10/17 depletion decreases the tumorigenic and migration potential of RB cells in vivo. Thus, ADAMs are potential novel targets for future therapeutic RB approaches.
Stichworte
retinoblastoma;
ADAM10;
ADAM17;
L1CAM;
CAM assay;
carcinogenesis;
tumorigenesis
Erscheinungsjahr
2022
Zeitschriftentitel
International Journal of Molecular Sciences
Band
23
Ausgabe
20
Art.-Nr.
12621
Urheberrecht / Lizenzen
eISSN
1422-0067
Page URI
https://pub.uni-bielefeld.de/record/2966985
Zitieren
Van Meenen D, Doege A, Alefeld E, et al. ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis. International Journal of Molecular Sciences. 2022;23(20): 12621.
Van Meenen, D., Doege, A., Alefeld, E., Haase, A., Beier, M., Kiefer, T., Biewald, E., et al. (2022). ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis. International Journal of Molecular Sciences, 23(20), 12621. https://doi.org/10.3390/ijms232012621
Van Meenen, Dario, Doege, Annika, Alefeld, Emily, Haase, Andre, Beier, Manfred, Kiefer, Tobias, Biewald, Eva, et al. 2022. “ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis”. International Journal of Molecular Sciences 23 (20): 12621.
Van Meenen, D., Doege, A., Alefeld, E., Haase, A., Beier, M., Kiefer, T., Biewald, E., Metz, K., Dräger, O., Busch, M. A., et al. (2022). ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis. International Journal of Molecular Sciences 23:12621.
Van Meenen, D., et al., 2022. ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis. International Journal of Molecular Sciences, 23(20): 12621.
D. Van Meenen, et al., “ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis”, International Journal of Molecular Sciences, vol. 23, 2022, : 12621.
Van Meenen, D., Doege, A., Alefeld, E., Haase, A., Beier, M., Kiefer, T., Biewald, E., Metz, K., Dräger, O., Busch, M.A., Dünker, N.: ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis. International Journal of Molecular Sciences. 23, : 12621 (2022).
Van Meenen, Dario, Doege, Annika, Alefeld, Emily, Haase, Andre, Beier, Manfred, Kiefer, Tobias, Biewald, Eva, Metz, Klaus, Dräger, Oliver, Busch, Maike Anna, and Dünker, Nicole. “ADAM10 and ADAM17-Novel Players in Retinoblastoma Carcinogenesis”. International Journal of Molecular Sciences 23.20 (2022): 12621.
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