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Favorable prognostic role of tropomodulins in neuroblastoma
Full text linkNeuroblastoma is a pediatric tumor of the sympatoadrenal lineage of the neural
crest characterized by high molecular and clinical heterogeneity, which are the main
causes of the poor response to standard multimodal therapy. The identification of new
and selective biomarkers is important to improve our knowledge on the mechanisms
of neuroblastoma progression and to find the targets for innovative cancer therapies.
This study identifies a positive correlation among tropomodulins (TMODs) proteins
expression and neuroblastoma progression. TMODs bind the pointed end of actin
filaments, regulate polymerization and depolymerization processes modifying actin
cytoskeletal dynamic and influencing neuronal development processes. Expression
levels of TMODs genes were analyzed in 17 datasets comprising different types
of tumors, including neuroblastoma, and it was demonstrated that high levels of
tropomodulin1 (TMOD1) and tropomodulin 2 (TMOD2) correlate positively with
high survival probability and with favorable clinical and molecular characteristics.
Functional studies on neuroblastoma cell lines, showed that TMOD1 knockin induced
cell cycle arrest, cell proliferation arrest and a mature functional differentiation.
TMOD1 overexpression was responsible for particular cell morphology and biochemical
changes which directed cells towards a neuronal favorable differentiation profile.
TMOD1 downregulation also induced cell proliferation arrest but caused the loss of
mature cell differentiation and promoted the development of neuroendocrine cellular
characteristics, delineating an aggressive and unfavorable tumor behavior. Overall,
these data indicated that TMODs are favorable prognostic biomarkers in neuroblastoma
and we believe that they could contribute to unravel a new pathophysiological
mechanism of neuroblastoma resistance contributing to the design of personalized
therapeutics opportunities
Cannabinoids in health and disease: Pharmacological potential in metabolic syndrome and neuroinflammation
No full textThe use of different natural and/or synthetic preparations of Cannabis sativa is associated with therapeutic strategies for many diseases. Indeed, thanks to the widespread diffusion of the cannabinoidergic system in the brain and in the peripheral districts, its stimulation, or inhibition, regulates many pathophysiological phenomena. In particular, central activation of the cannabinoidergic system modulates the limbic and mesolimbic response which leads to food craving. Moreover, cannabinoid agonists are able to reduce inflammatory response. In this review a brief history of cannabinoids and the protagonists of the endocannabinoidergic system, i.e. synthesis and degradation enzymes and main receptors, will be described. Furthermore, the pharmacological effects of cannabinoids will be outlined. An overview of the involvement of the endocannabinoidergic system in neuroinflammatory and metabolic pathologies will be made. Finally, particular attention will also be given to the new pharmacological entities acting on the two main receptors, cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2), with particular focus on the neuroinflammatory and metabolic mechanisms involved
Mitochondrial dysfunction and increased sensitivity to excitotoxicity in mice deficient in DNA mismatch repair
No full textA novel mechanism for pergolide-induced neuroprotection: inhibition of NF-kappaB nuclear translocation
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