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Your search keyword '"Naselli, F"' showing total 3 results
Start Over Author "Naselli, F" Publisher nature publishing group
3 results on '"Naselli, F"'

1. Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

Author

Laura Saieva, Christian Rolfo, Giovanni Zito, Stefano Forte, Claudio Guzzardo, Stefania Raimondo, Giovanna Calabrese, Flores Naselli, Riccardo Alessandro, Rosalba Parenti, Zito, G., Naselli, F., Saieva, L., Raimondo, S., Calabrese, G., Guzzardo, C., Forte, S., Rolfo, C., Parenti, R., and Alessandro, R.

Subjects
0301 basic medicine, Acute promyelocytic leukemia, Science, EGFR, Retinoic acid, Mice, Nude, Tretinoin, Biology, Article, 03 medical and health sciences, chemistry.chemical_compound, Differentiation therapy, Settore BIO/13 - Biologia Applicata, Carcinoma, Non-Small-Cell Lung, Cell Line, Tumor, GATA6 Transcription Factor, medicine, Animals, Humans, Lung cancer, Protein Kinase Inhibitors, Wnt Signaling Pathway, Transcription factor, Cell Proliferation, Multidisciplinary, Wnt signaling pathway, Cell Differentiation, medicine.disease, G1 Phase Cell Cycle Checkpoints, Xenograft Model Antitumor Assays, respiratory tract diseases, ErbB Receptors, lung cancer, Drug Resistance, Neoplasm, Signal Transduction, 030104 developmental biology, chemistry, Immunology, Cancer research, Medicine, Adenocarcinoma, Engineering sciences. Technology, Tyrosine kinase
Abstract

A fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved in the physiological differentiation of the distal lung. In addition, our results demonstrate that RA inhibits EGFR and Wnt signaling activation, two pathways involved in NSCLC progression. Furthermore, we uncovered a novel mechanism in NSCLC that shows how RA exerts its function; we found that RA-mediated GATA6 activation is necessary for EGFR and Wnt inhibition, thus leading to 1) increased differentiation and 2) loss of proliferation. All together, these findings prove that differentiation therapy might be feasible in TKI resistant NSCLCs, and shed light on new targets to define new pharmacological therapies.

Published
2017

2. Nutritional epigenomic and DNA-damage modulation effect of natural stilbenoids.

Author

Volpes S, Cruciata I, Ceraulo F, Schimmenti C, Naselli F, Pinna C, Mauro M, Picone P, Dallavalle S, Nuzzo D, Pinto A, and Caradonna F

Subjects
Humans, Resveratrol, Caco-2 Cells, Epigenomics, Stilbenes pharmacology, Vitis
Abstract

The aim of the present work is the evaluation of biological effects of natural stilbenoids found in Vitis vinifera, with a focus on their activity as epigenetic modulators. In the present study, resveratrol, pterostilbene and for the first time their dimers (±)-trans-δ-viniferin, (±)-trans-pterostilbene dehydrodimer were evaluated in Caco-2 and HepG-2 cell lines as potential epigenetic modulators. Stilbenoids were added in a Caco-2 cell culture as a model of the intestinal epithelial barrier and in the HepG-2 as a model of hepatic environment, to verify their dose-dependent toxicity, ability to interact with DNA, and epigenomic action. Resveratrol, pterostilbene, and (±)-trans-pterostilbene dehydrodimer were found to have no toxic effects at tested concentration and were effective in reversing arsenic damage in Caco-2 cell lines. (±)-trans-δ-viniferin showed epigenomic activity, but further studies are needed to clarify its mode of action., (© 2023. The Author(s).)

Published
2023
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3. Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition.

Author

Zito G, Naselli F, Saieva L, Raimondo S, Calabrese G, Guzzardo C, Forte S, Rolfo C, Parenti R, and Alessandro R

Subjects
Animals, Carcinoma, Non-Small-Cell Lung genetics, Cell Differentiation drug effects, Cell Line, Tumor, Cell Proliferation drug effects, Drug Resistance, Neoplasm genetics, ErbB Receptors antagonists & inhibitors, G1 Phase Cell Cycle Checkpoints drug effects, GATA6 Transcription Factor metabolism, Humans, Mice, Nude, Protein Kinase Inhibitors pharmacology, Signal Transduction drug effects, Xenograft Model Antitumor Assays, Carcinoma, Non-Small-Cell Lung drug therapy, ErbB Receptors drug effects, GATA6 Transcription Factor drug effects, Tretinoin pharmacology, Wnt Signaling Pathway drug effects
Abstract

A fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved in the physiological differentiation of the distal lung. In addition, our results demonstrate that RA inhibits EGFR and Wnt signaling activation, two pathways involved in NSCLC progression. Furthermore, we uncovered a novel mechanism in NSCLC that shows how RA exerts its function; we found that RA-mediated GATA6 activation is necessary for EGFR and Wnt inhibition, thus leading to 1) increased differentiation and 2) loss of proliferation. All together, these findings prove that differentiation therapy might be feasible in TKI resistant NSCLCs, and shed light on new targets to define new pharmacological therapies.

Published
2017
Full Text
View/download PDF

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