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- Unravelling the formation of a palmelloid-like phenotype in the green microalga Raphidocelis subcapitata when exposed to pollutantsPublication . Machado. Manuela dias; Soares, Eduardo Valente; Raldúa, DemetrioIntroduction: Unicellular microorganisms may present different defence and survival strategies, when exposed to pollutants or adverse environments. For instance, the microalgae belonging to the genera Chlamydomonas, Chlorella, and Dunaliella, in response to high salinity or toxics, can form a structure (comprising non-motile cells surrounded by a matrix of polysaccharides) called “palmelloid”, due to its similarity with the morphology of the alga Palmella. Objectives: This work aimed to verify the formation of a palmelloid-like (multinucleated) phenotype in the freshwater microalgae Raphidocelis subcapitata caused by exposure to inorganic or organic pollutants. The kinetics of the formation of the palmelloid-like phenotype and its reversibility were also studied. Methods: The microalga was incubated with heavy metals (Cd or Zn) and organic compounds (the antibiotic erythromycin (ERY) or the herbicide metolachlor (MET)) at various concentrations. After 24, 48, and 72 h, the palmelloid-like phenotype formation was evaluated. Results: In the absence of stress or when exposed to ERY or Zn up to 200 µgL-1 (where growth was reduced or halted), R. subcapitata exhibited, primarily, a single nucleus. At sub-lethal and environmentally relevant concentrations of MET (100-200 µgL-1) or Cd (200 µgL-1), the alga transitioned to a multinucleated state, similar to the “palmelloid” morphology observed in different green algae. The multinucleated state was reversed when the microalgae were re-inoculated in a fresh medium (without pollutants). Conclusions: The development of a palmelloid-like phenotype in R. subcapitata when exposed to sub-lethal levels of inorganic or organic pollutants is not a universal defence and response strategy to stress, as it depends on the pollutant, its concentration, and the duration of the exposure. The multinucleated state is a reversible process. The insights provided in this study contribute to increasing the knowledge of the strategies used by R. subcapitata to manage severe stress induced by pollutants.
- Unraveling the significance of DGCR8 and miRNAs in thyroid carcinomaPublication . Rodrigues, Lia; Paula, Arnaud Da Cruz; Soares, Paula; Vinagre, JoãoMicroRNAs (miRNAs) act as negative regulators for protein-coding gene expression impacting cell proliferation, differentiation, and survival. These miRNAs are frequently dysregulated in cancer and constitute classes of blood-based biomarkers useful for cancer detection and prognosis definition. In thyroid cancer (TC), the miRNA biogenesis pathway plays a pivotal role in thyroid gland formation, ensuring proper follicle development and hormone production. Several alterations in the miRNA biogenesis genes are reported as a causality for miRNA dysregulation. Mutations in microprocessor component genes are linked to an increased risk of developing TC; in particular, a recurrent mutation affecting DGCR8, the E518K. In this review, we explore these novel findings and resume the current state-of-the-art in miRNAs in thyroid carcinomas.
- Glucose metabolism as a potential therapeutic target in Cytarabine-resistant acute Myeloid leukemiaPublication . Pereira-Vieira, Joana; Weber, Daniela D.; Silva, Sâmia; Barbosa-Matos, Catarina; Granja, Sara; Reis, Rui Manuel; Queirós, Odília; Ko, Young H.; Kofler, Barbara; Casal, Margarida; Baltazar, Fátima; Granja, SaraAltered glycolytic metabolism has been associated with chemoresistance in acute myeloid leukemia (AML). However, there are still aspects that need clarification, as well as how to explore these metabolic alterations in therapy. In the present study, we aimed to elucidate the role of glucose metabolism in the acquired resistance of AML cells to cytarabine (Ara-C) and to explore it as a therapeutic target. Resistance was induced by stepwise exposure of AML cells to increasing concentrations of Ara-C. Ara-C-resistant cells were characterized for their growth capacity, genetic alterations, metabolic profile, and sensitivity to different metabolic inhibitors. Ara-C-resistant AML cell lines, KG-1 Ara-R, and MOLM13 Ara-R presented different metabolic profiles. KG-1 Ara-R cells exhibited a more pronounced glycolytic phenotype than parental cells, with a weaker acute response to 3-bromopyruvate (3-BP) but higher sensitivity after 48 h. KG-1 Ara-R cells also display increased respiration rates and are more sensitive to phenformin than parental cells. On the other hand, MOLM13 Ara-R cells display a glucose metabolism profile similar to parental cells, as well as sensitivity to glycolytic inhibitors. These results indicate that acquired resistance to Ara-C in AML may involve metabolic adaptations, which can be explored therapeutically in the AML patient setting who developed resistance to therapy.