Please use this identifier to cite or link to this item: https://scholarhub.balamand.edu.lb/handle/uob/2184
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dc.contributor.authorRached, Johnnyen_US
dc.contributor.authorNasr, Zeinaen_US
dc.contributor.authorAbdallah, Jaden_US
dc.contributor.authorAbou-Antoun, Tamaraen_US
dc.date.accessioned2020-12-23T09:08:05Z-
dc.date.available2020-12-23T09:08:05Z-
dc.date.issued2016-
dc.identifier.urihttps://scholarhub.balamand.edu.lb/handle/uob/2184-
dc.description.abstractChildhood neuroblastoma is one of the most malignant types of cancers leading to a high mortality rate. These cancerous cells can be highly metastatic and malignant giving rise to disease recurrence and poor prognosis. The proto-oncogene myelocytomatosis neuroblastoma (MycN) is known to be amplified in this type of cancer, thus, promoting high malignancy and resistance. The L1 cell adhesion molecule (L1-CAM) cleavage has been found upregulated in many types of malignant cancers. In the present study, we explored the interplay between L1-CAM, MycN and PTEN as well as the role played by PDGFR and VEGFR on tumorigenicity in neuroblastoma cells. We investigated the effect of L1-CAM knock-down (KD) and PDGFR/VEGFR inhibition with sunitinib malate (Sutent®) treatment on subsequent tumorsphere formation and cellular proliferation and migration in the MycN-amplified IMR-32 neuroblastoma cells. We further examined the effect of combined L1-CAM KD with Sutent treatment or radiotherapy on these cellular functions in our cells. Tumorsphere formation is one of the indicators of aggressiveness in malignant cancers, which was significantly inhibited in IMR-32 cells after L1-CAM KD or Sutent treatment, however, no synergistic effect was observed with dual treatments, rather L1-CAM KD alone showed a greater inhibition on tumorsphere formation compared to Sutent treatment alone. In addition, cellular proliferation and migration were significantly inhibited after L1-CAM KD in the IMR-32 cells with no synergistic effect observed on the rate of cell proliferation when combined with Sutent treatment. Again, L1-CAM KD alone exhibited greater inhibitory effect than Sutent treatment on cell proliferation. L1-CAM KD led to the simultaneous downregulation of MycN, but the upregulation of PTEN protein expression. Notably, radiotherapy (2 Gy) of the IMR-32 cells led to significant upregulation of both L1-CAM and MycN, which was abrogated with L1-CAM KD in our cells. In addition, L1-CAM KD radio.en_US
dc.format.extent7 p.en_US
dc.language.isoengen_US
dc.titleL1-CAM knock-down radiosensitizes neuroblastoma IMR-32 cells by simultaneously decreasing MycN, but increasing PTEN protein expressionen_US
dc.typeJournal Articleen_US
dc.identifier.doi10.3892/ijo.2016.3625-
dc.contributor.affiliationDepartment of Biologyen_US
dc.description.volume9en_US
dc.description.startpage1722en_US
dc.description.endpage1730en_US
dc.date.catalogued2017-11-03-
dc.description.statusPublisheden_US
dc.identifier.OlibID174722-
dc.identifier.openURLhttps://doi.org/10.3892/ijo.2016.3625en_US
dc.relation.ispartoftextJournal of oncologyen_US
dc.provenance.recordsourceOliben_US
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