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3,5,3’ Triiodo-l-thyronine prevents pancreatic β cell death via nongenomic activation of pi3k signaling pathway
Full text linkThe thyroid hormone T3 improves function and survival of rat pancreatic islets during in vitro culture
No full textO2/3 exposure inhibits cell progression affecting cyclin B1/cdk 1 activity in SK-N-SH while induces apoptosis in SK-N-DZ neuroblastoma cells
No full textIn search for innovative therapeutic agents for children neuroblastoma, the oxygen therapy could be considered an alternative antitumoral
treatment. Given the physiochemical properties ofO2/3 gas mixture including fairly low aqueous solubility and spreading, and the
interesting perspective of hyperoxia, we analyzed the inhibitory effect ofO2/3 treatment on two human neuroblastoma cell lines (SK-N-SH
and SK-N-DZ). In this study, we demonstrated thatO2/3 treatment was able to induce cell growth inhibition and cell cycle perturbation in
both cell lines. We observed an arrest at G2 phase, accompanied by an alteration in the expression and localization of cyclin B1/cdk1
complex and a reduction in its activity in SK-N-SH cells. This reduction was consistent with the increase in both Wee1 and chk1 protein
levels. On the contrary, O2/3 induced apoptosis in SK-N-DZ cells via caspase 3 activation and Poly ADP-ribose polymerase-1 (PARP)
cleavage, associated with an increase in the pro-apoptotic Bax protein. Consequently, we considered the possibility of improving the
responsiveness to chemotherapeutic agents such as Cisplatin, Etoposide, and Gemcitabine in combination with O2/3 treatment. The
combined treatments produced a stronger cell inhibitory effect than Cisplatin and Etoposide used alone in SK-N-SH cells.Onthe contrary,
the combination data were not significantly different from O2/3 treatment alone in SK-N-DZ cells, thus suggesting that the obtained
changes in cell growth inhibition were due to the effect of O2/3 alone
Identificazione di geni pancreatici regolati dagli ormoni tiroidei mediante cDNA microarray
No full text
The Thyroid Hormone T3 Improves Function and Survival of Rat Pancreatic Islets during In Vitro Culture.
No full textThyroid hormones enhance growth and counteract apoptosis in human tenocytes isolated from rotator cuff tendons
No full text[No abstract available
Role of the 3,5,3'-triodo-l-thyronine in the process of differentiation of a human pancreatic duct cell line
No full textPoster Presentation Abs no. P29. JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION. Impact Factor = 1.59
Thyroid hormones inhibit cell proliferation and induce differentiation of human pancreatic ductal cells into insulin secreting cells
No full textOral presentation Abs no. OC23. JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION. Impact Factor = 1.59
Myc down-regulation affects cyclin D1/cdk4 activity and induces apoptosis via Smac/Diablo pathway in astrocytoma cell lines
No full textOBJECTIVES: We investigated the antiproliferative effect of Myc down-regulation via cell proliferation inhibition, cell cycle perturbation and apoptosis in two human astrocytoma models (T98G and ADF) steadily expressing an inducible c-myc Anti-sense RNA. MATERIALS AND METHODS: Cell growth experiments were performed using the trypan blue dye exclusion test and cell cycle analysis was evaluated by flow cytometry. Cell cycle molecules were detected by Western blot analysis, co-immunoprecipitation and reverse transcription-polymerase chain reaction assays. RESULTS: We showed that Myc down-regulation in astrocytoma cells led to G1 accumulation and an inhibition of cell proliferation characterized by S phase delay. Co-immunoprecipitation experiments detected formation of inactive cyclin D1/cdk4 complexes as evaluated by presence of an active unphosphorylated form of retinoblastoma protein, the best characterized target substrate for cyclin D1/cdk4 complex, in ADF pINDc-myc anti-sense 7 cells. We also found that either p57Kip2 "apice" or p27Kip1 "apice" inhibitors bound to cyclin D1/cdk4 complex, thus, suggesting that they cooperated to inhibit the activity of cyclin D1/cdk4. Moreover, c-Myc down-regulation led to activation of the apoptotic mitochondrial pathway, characterized by release of cytochrome c and Smac/Diablo proteins and by reduction of c-IAP levels through activation of proteasome-mediated protein degradation system. CONCLUSIONS: Our results suggest that c-Myc could be considered as a good target for the study of new approaches in anticancer astrocytoma treatment
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