Browsing by Author "Matos, Alexandra Sofia Soares Curado de"
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- Unveiling a potential role for CITED2 in Glioblastoma BiologyPublication . Matos, Alexandra Sofia Soares Curado de; Fernandes , Mónica Teotónio; Bragança, JoséThe most prevalent and severe malignant brain tumor, glioblastoma (GBM), is marked by a high rate of brain invasion, resistance to treatment, and an overall poor prognosis. A heterogeneous population of cells, including a subpopulation of more undifferentiated cells called glioblastoma stem-like cells, make up these tumors. This subpopulation may be the source of therapy resistance and relapse, thus targeting these cells may be more successful. Therefore, it is essential to comprehend the biology of these cells in order to identify potential therapeutic targets. In both adult and embryonic stem cells, CITED2 is a crucial pluripotency factor and a co-transcriptional modulator. Furthermore, it has been linked to a number of cancer types, having either pro- or anti-tumorigenic roles. However, a possible role in GBM has not yet been documented. Thus, the objective of this study was to determine the impact of CITED2 modulation on the biology of GBM. Three GBM cell lines were selected for this investigation to assess the effect of CITED2 expression. Concerning the modification of CITED2, clones in GBM cell line models that had both overexpression and knockdown of CITED2 were created. We observed effects on the metabolic activity, proliferation, migration, cell cycle progression, cell death, clonogenic potential, tumorigenic potential and invasion when CITED2 was overexpressed and knocked down. Taken together, the present study on CITED2 biology suggests a potential role in glioblastoma. The ability to self-renew, the metabolic activity, clonogenic and tumorigenic potential, cell death and invasion are all indicators of this effect. Considering the results of this study, it will be important to further investigate the specific role of CITED2 in GBM cell biology and to explore whether CITED2 itself or the pathways activated by CITED2 could serve as potential therapeutic targets.