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3. Evidence of the Link between Stroma Remodeling and Prostate Cancer Prognosis.

Author

Vecchiotti, Davide, Clementi, Letizia, Cornacchia, Emanuele, Di Vito Nolfi, Mauro, Verzella, Daniela, Capece, Daria, Zazzeroni, Francesca, and Angelucci, Adriano

Subjects
EPITHELIAL cells, CANCER, CONNECTIVE tissue cells, PROSTATE tumors, TUMOR markers, MUSCLE cells, ENERGY metabolism, FIBROBLASTS, EXTRACELLULAR matrix, MOLECULAR biology, CELL differentiation
Abstract

Simple Summary: Prostate cancer (PCa) is among the most common cancers. While PCa is frequently diagnosed in elderly men as a slow-growing, low-risk disease, in about 10–15% of cases, it can become a life-threatening danger. Unfortunately, biomarkers able to discriminate indolent prostatic tumors from aggressive forms are lacking, and watchful waiting remains one of the best options. However, available data support the hypothesis that distinctive biological characteristics of PCa stroma can contribute to cancer progression in a clinically relevant way. According to the current view, tissue alterations induced by tumor growth affect both metabolism of resident normal cells and composition of the extracellular matrix and are able also to recruit cells from circulation. Here, we seek to respond to the challenge of identifying stroma-associated biomarkers that may be relevant to assist prognostic decisions in PCa patients. Prostate cancer (PCa), the most commonly diagnosed cancer in men worldwide, is particularly challenging for oncologists when a precise prognosis needs to be established. Indeed, the entire clinical management in PCa has important drawbacks, generating an intense debate concerning the possibility to individuate molecular biomarkers able to avoid overtreatment in patients with pathological indolent cancers. To date, the paradigmatic change in the view of cancer pathogenesis prompts to look for prognostic biomarkers not only in cancer epithelial cells but also in the tumor microenvironment. PCa ecology has been defined with increasing details in the last few years, and a number of promising key markers associated with the reactive stroma are now available. Here, we provide an updated description of the most biologically significant and cited prognosis-oriented microenvironment biomarkers derived from the main reactive processes during PCa pathogenesis: tissue adaptations, inflammatory response and metabolic reprogramming. Proposed biomarkers include factors involved in stromal cell differentiation, cancer-normal cell crosstalk, angiogenesis, extracellular matrix remodeling and energy metabolism. [ABSTRACT FROM AUTHOR]

Published
2024
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4. A method to comprehensively identify germline SNVs, INDELs and CNVs from whole exome sequencing data of BRCA1/2 negative breast cancer patients

Author

Bianchi, Andrea, primary, Zelli, Veronica, additional, D’Angelo, Andrea, additional, Di Matteo, Alessandro, additional, Scoccia, Giulia, additional, Cannita, Katia, additional, Dimas, Antigone S, additional, Glentis, Stavros, additional, Zazzeroni, Francesca, additional, Alesse, Edoardo, additional, Di Marco, Antinisca, additional, and Tessitore, Alessandra, additional

Published
2024
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5. NF-κB: Governing Macrophages in Cancer

Author

Cornice, Jessica, primary, Verzella, Daniela, additional, Arboretto, Paola, additional, Vecchiotti, Davide, additional, Capece, Daria, additional, Zazzeroni, Francesca, additional, and Franzoso, Guido, additional

Published
2024
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12. Bi-allelic genetic variants in the translational GTPases GTPBP1 and GTPBP2 cause a distinct identical neurodevelopmental syndrome

Author

Hannah, Michael G., Bugiardini, Enrico, Bertini, Enrico, Kriouile, Yamna, El-Khorassani, Mohamed, Aguennouz, Mhammed, Groppa, Stanislav, Karashova, Blagovesta M., Goraya, Jatinder S., Sultan, Tipu, Avdjieva, Daniela, Kathom, Hadil, Tincheva, Radka, Banu, Selina, Veggiotti, Pierangelo, Verrotti, Alberto, Lanari, Marcello, Savasta, Salvatore, Macaya, Alfons, Garavaglia, Barbara, Borgione, Eugenia, Papacostas, Savvas, Vikelis, Michail, Chelban, Viorica, Kaiyrzhanov, Rauan, Cortese, Andrea, Sullivan, Roisin, Papanicolaou, Eleni Z., Dardiotis, Efthymios, Maqbool, Shazia, Ibrahim, Shahnaz, Kirmani, Salman, Rana, Nuzhat N., Atawneh, Osama, Lim, Shen-Yang, Zuccotti, Gian V., Marseglia, Gian L., Esposito, Susanna, Shaikh, Farooq, Cogo, Paola, Corsello, Giovanni, Mangano, Salvatore, Nardello, Rosaria, Mangano, Donato, Scardamaglia, Annarita, Koutsis, George, Scuderi, Carmela, Ferrara, Pietro, Morello, Giovanna, Zollo, Massimo, Berni-Canani, Roberto, Terracciano, Luigi M., Sisto, Antonio, Di Fabio, Sandra, Strano, Federica, Scorrano, Giovanna, Di Bella, Saverio, Di Francesco, Ludovica, Manizha, Ganieva, Isrofilov, Maksud, Guliyeva, Ulviyya, Salayev, Kamran, Khachatryan, Samson, Xiromerisiou, Georgia, Spanaki, Cleanthe, Fiorillo, Chiara, Iacomino, Michele, Gaudio, Eugenio, Munell, Francina, Gagliano, Antonella, Jan, Farida, Chimenz, Roberto, Gitto, Eloisa, Iughetti, Lorenzo, Di Rosa, Gabriella, Maghnie, Mohamad, Pettoello-Mantovani, Massimo, Gupta, Neerja, Kabra, Madhulika, Benrhouma, Hanene, Tazir, Meriem, Bottone, Gabriella, Farello, Giovanni, Delvecchio, Maurizio, Di-Donato, Giulio, Obeid, Makram, Bakhtadze, Sophia, Saadi, Nebal W., Miraglia-Del-Giudice, Michele, Maccarone, Rita, Zaki, Maha S., Triki, Chahnez C., Kara, Majdi, Karimiani, Ehsan G., Salih, Ahmed M., Ramenghi, Luca A., Seri, Marco, Di-Falco, Giovanna, Mandarà, Luana, Barrano, Giuseppe, Elisa, Maurizio, Cherubini, Enrico, Operto, Francesca F., Valenzise, Mariella, Cattaneo, Antonino, Zazzeroni, Francesca, Alesse, Edoardo, Matricardi, Sara, Zafar, Faisal, Ullah, Ehsan, Afzal, Erum, Rahman, Fatima, Ahmed, Muhammad M., Parisi, Pasquale, Spalice, Alberto, De Filippo, Maria, Licari, Amelia, Trebbi, Edoardo, Romano, Ferdinando, Heimer, Gali, Al-Khawaja, Issam, Al-Mutairi, Fuad, Alkuraya, Fowzan S., Rizig, Mie, Shashkin, Chingiz, Zharkynbekova, Nazira, Koneyev, Kairgali, Salpietro, Vincenzo, Maroofian, Reza, Wangen, Jamie, Ciolfi, Andrea, Barresi, Sabina, Efthymiou, Stephanie, Lamaze, Angelique, Aughey, Gabriel N., Al Mutairi, Fuad, Rad, Aboulfazl, Rocca, Clarissa, Calì, Elisa, Accogli, Andrea, Zara, Federico, Striano, Pasquale, Mojarrad, Majid, Tariq, Huma, Giacopuzzi, Edoardo, Taylor, Jenny C., Oprea, Gabriela, Skrahina, Volha, Rehman, Khalil Ur, Abd Elmaksoud, Marwa, Bassiony, Mahmoud, El Said, Huda G., Abdel-Hamid, Mohamed S., Al Shalan, Maha, Seo, Gohun, Kim, Sohyun, Lee, Hane, Khang, Rin, Issa, Mahmoud Y., Elbendary, Hasnaa M., Rafat, Karima, Marinakis, Nikolaos M., Traeger-Synodinos, Joanne, Ververi, Athina, Sourmpi, Mara, Eslahi, Atieh, Khadivi Zand, Farhad, Beiraghi Toosi, Mehran, Babaei, Meisam, Jackson, Adam, Bertoli-Avella, Aida, Pagnamenta, Alistair T., Niceta, Marcello, Battini, Roberta, Corsello, Antonio, Leoni, Chiara, Chiarelli, Francesco, Dallapiccola, Bruno, Faqeih, Eissa Ali, Tallur, Krishnaraya K., Alfadhel, Majid, Alobeid, Eman, Maddirevula, Sateesh, Mankad, Kshitij, Banka, Siddharth, Ghayoor-Karimiani, Ehsan, Tartaglia, Marco, Chung, Wendy K., Green, Rachel, Jepson, James E.C., and Houlden, Henry

Published
2024
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13. MiR-182-5p Is Upregulated in Hepatic Tissues from a Diet-Induced NAFLD/NASH/HCC C57BL/6J Mouse Model and Modulates Cyld and Foxo1 Expression

Author

Compagnoni, Chiara, primary, Capelli, Roberta, additional, Zelli, Veronica, additional, Corrente, Alessandra, additional, Vecchiotti, Davide, additional, Flati, Irene, additional, Di Vito Nolfi, Mauro, additional, Angelucci, Adriano, additional, Alesse, Edoardo, additional, Zazzeroni, Francesca, additional, and Tessitore, Alessandra, additional

Published
2023
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20. NF-κB: A Druggable Target in Acute Myeloid Leukemia

Author

Di Francesco, Barbara, primary, Verzella, Daniela, additional, Capece, Daria, additional, Vecchiotti, Davide, additional, Di Vito Nolfi, Mauro, additional, Flati, Irene, additional, Cornice, Jessica, additional, Di Padova, Monica, additional, Angelucci, Adriano, additional, Alesse, Edoardo, additional, and Zazzeroni, Francesca, additional

Published
2022
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22. Elevated NF-κB/SHh/GLI1 Signature Denotes a Worse Prognosis and Represent a Novel Potential Therapeutic Target in Advanced Prostate Cancer

Author

Vecchiotti, Davide, primary, Verzella, Daniela, additional, Di Vito Nolfi, Mauro, additional, D’Andrea, Daniel, additional, Flati, Irene, additional, Di Francesco, Barbara, additional, Cornice, Jessica, additional, Alesse, Edoardo, additional, Capece, Daria, additional, and Zazzeroni, Francesca, additional

Published
2022
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25. MicroRNAs Expression in Response to rhNGF in Epithelial Corneal Cells: Focus on Neurotrophin Signaling Pathway

Author

Compagnoni, Chiara, primary, Zelli, Veronica, additional, Bianchi, Andrea, additional, Di Marco, Antinisca, additional, Capelli, Roberta, additional, Vecchiotti, Davide, additional, Brandolini, Laura, additional, Cimini, Anna Maria, additional, Zazzeroni, Francesca, additional, Allegretti, Marcello, additional, Alesse, Edoardo, additional, and Tessitore, Alessandra, additional

Published
2022
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26. Role of exosomal microRNAs in cancer therapy and drug resistance mechanisms: focus on hepatocellular carcinoma

Author

Zelli, Veronica, Compagnoni, Chiara, Capelli, Roberta, Corrente, Alessandra, Di Vito Nolfi, Mauro, Zazzeroni, Francesca, Alesse, Edoardo, and Tessitore, Alessandra

Subjects
Cancer Research, therapy, drug resistance, Oncology, exosomes, hepatocellular carcinoma, miRNAs
Abstract

Extracellular vesicles (EVs), defined as intercellular messengers that carry their cargos between cells, are involved in several physiological and pathological processes. These small membranous vesicles are released by most cells and contain biological molecules, including nucleic acids, proteins and lipids, which can modulate signaling pathways of nearby or distant recipient cells. Exosomes, one the most characterized classes of EVs, include, among others, microRNAs (miRNAs), small non-coding RNAs able to regulate the expression of several genes at post-transcriptional level. In cancer, exosomal miRNAs have been shown to influence tumor behavior and reshape tumor microenvironment. Furthermore, their possible involvement in drug resistance mechanisms has become evident in recent years. Hepatocellular carcinoma (HCC) is the major type of liver cancer, accounting for 75-85% of all liver tumors. Although the improvement in HCC treatment approaches, low therapeutic efficacy in patients with intermediate-advanced HCC is mainly related to the development of tumor metastases, high risk of recurrence and drug resistance. Exosomes have been shown to be involved in pathogenesis and progression of HCC, as well as in drug resistance, by regulating processes such as cell proliferation, epithelial-mesenchymal transition and immune response. Herein, we summarize the current knowledge about the involvement of exosomal miRNAs in HCC therapy, highlighting their role as modulators of therapeutic response, particularly chemotherapy and immunotherapy, as well as possible therapeutic tools.

Published
2022

27. Concurrent RAS and RAS/BRAF V600E variants in colorectal cancer: more frequent than expected?

Author

Zelli, Veronica, Parisi, Alessandro, Patruno, LEONARDO VALERIO, Katia, Cannita, Ficorella, Corrado, Luzi, Carla, Compagnoni, Chiara, Zazzeroni, Francesca, Alesse, Edoardo, and Tessitore, Alessandra

Subjects
concurrent RAS/BRAF variants, colorectal cancer, concurrent RAS/BRAF variants, case report, mutation frequency, Q9 clinical–pathological features, Q9 clinical–pathological features, case report, colorectal cancer, mutation frequency
Published
2022

29. Ultrasound-Based Method for the Identification of Novel MicroRNA Biomarkers in Prostate Cancer

Author

Cornice, Jessica, primary, Capece, Daria, additional, Di Vito Nolfi, Mauro, additional, Di Padova, Monica, additional, Compagnoni, Chiara, additional, Verzella, Daniela, additional, Di Francesco, Barbara, additional, Vecchiotti, Davide, additional, Flati, Irene, additional, Tessitore, Alessandra, additional, Alesse, Edoardo, additional, Barbato, Gaetano, additional, and Zazzeroni, Francesca, additional

Published
2021
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31. The glycosaminoglycan-binding domain of PRELP acts as a cell type-specific NF-[kappa]B inhibitor that impairs osteoclastogenesis

Author

Rucci, Nadia, Rufo, Anna, Alamanou, Marina, Capulli, Mattia, Del Fattore, Andrea, Ahrman, Emma, Capece, Daria, Iansante, Valeria, Zazzeroni, Francesca, Alesse, Edoardo, Heinegard, Dick, and Teti, Anna

Subjects
Glycosaminoglycans -- Physiological aspects, Gene expression -- Physiological aspects, Biological sciences
Abstract

Proline/arginine-rich end leucine-rich repeat protein (PRELP) is a glycosaminoglycan (GAG)- and collagen-binding anchor protein highly expressed in cartilage, basement membranes, and developing bone. We observed that PRELP inhibited in vitro and in vivo mouse osteoclastogenesis through its GAG-binding domain ([sup.hbd]PRELP), involving (a) cell internalization through a chondroitin sulfate- and annexin Il-dependent mechanism, (b) nuclear translocation, (c) interaction with p65 nuclear factor [kappa]B (NF-[kappa]B) and inhibition of its DNA binding, and (d) impairment of NF-[kappa]B transcriptional activity and reduction of osteoclast-specific gene expression, [sup.hbd]PRELP does not disrupt the mitogen-activated protein kinase signaling nor does it impair cell survival, [sup.hbd]PRELP activity is cell type specific, given that it is internalized by the RAW264.7 osteoclast-like cell line but fails to affect calvarial osteoblasts, bone marrow macrophages, and epithelial cell lines. In vivo, hbdpRELP reduces osteoclast number and activity in ovariectomized mice, underlying its physiological and/or pathological importance in skeletal remodeling. doi/10.1083/jcb.200906014

Published
2009

32. Gadd45[beta] promotes hepatocyte survival during liver regeneration in mice by modulating JNK signaling

Author

Papa, Salvatore, Zazzeroni, Francesca, Fu, Yang-Xin, Bubici, Concetta, Alvarez, Kellean, Dean, Kathryn, Christiansen, Peter A., Anders, Robert A., and Franzoso, Guido

Subjects
Liver cells -- Health aspects, Liver cells -- Genetic aspects, Liver cells -- Research, Liver -- Regeneration, Liver -- Physiological aspects, Liver -- Genetic aspects, Liver -- Research
Abstract

In the liver, the JNK cascade is induced downstream of TNF receptors (TNFRs) in response to inflammatory, microbial, and toxic challenges. Sustained activation of JNK triggers programmed cell death (PCD), and hepatocyte survival during these challenges requires induction of the NF-[kappa]B pathway, which antagonizes this activation by upregulating target genes. Thus, modulation of JNK activity is crucial to the liver response to TNFR-mediated challenge. The basis for this modulation, however, is unknown. Here, we investigated the role of the NF-[kappa]B target Gadd45b in the regulation of hepatocyte fate during liver regeneration after partial hepatectomy. We generated Gadd45b-/- mice and found that they exhibited decreased hepatocyte proliferation and increased PCD during liver regeneration. Notably, JNK activity was markedly increased and sustained in livers of Gadd45b-/- mice compared with control animals after partial hepatectomy. Furthermore, imposition of a Jnk2-null mutation, attenuating JNK activity, completely rescued the regenerative response in Gadd45b-/- mice. Interestingly, Gadd45[beta] ablation did not affect hepatotoxic JNK signaling after a TNFR-mediated immune challenge, suggesting specificity in the inducible hepatic program for JNK restraint activated during distinct TNFR-mediated challenges. These data provide a basis for JNK suppression during liver regeneration and identify Gadd45[beta] as a potential therapeutic target in liver diseases., Introduction TNF-[alpha] is a pleiotropic cytokine that plays important roles in immunity, inflammation, and tumorigenesis (1), (2). Exposure to TNF-[alpha] induces either cell proliferation or programmed cell death (PCD) through [...]

Published
2008

33. Low Radiation Environment Switches the Overgrowth-Induced Cell Apoptosis Toward Autophagy

Author

Fischietti, Mariafausta, primary, Fratini, Emiliano, additional, Verzella, Daniela, additional, Vecchiotti, Davide, additional, Capece, Daria, additional, Di Francesco, Barbara, additional, Esposito, Giuseppe, additional, Balata, Marco, additional, Ioannuci, Luca, additional, Sykes, Pamela, additional, Satta, Luigi, additional, Zazzeroni, Francesca, additional, Tessitore, Alessandra, additional, Tabocchini, Maria Antonella, additional, and Alesse, Edoardo, additional

Published
2021
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35. [REN.sup.KCTD11] is a suppressor of Hedgehog signaling and is deleted in human medulloblastoma

Author

Di Marcotullio, Lucia, Ferretti, Elisabetta, De Smaele, Enrico, Argenti, Beatrice, Mincione, Claudia, Zazzeroni, Francesca, Gallo, Rita, Masuelli, Laura, Napolitano, Maddalena, Maroder, Marella, Modesti, Andrea, Giangaspero, Felice, Screpanti, Isabella, Alesse, Edoardo, and Gulino, Alberto

Subjects
Oncology -- Research, Science and technology
Abstract

Hedgehog signaling is suggested to be a major oncogenic pathway in medulloblastoma, which arises from aberrant development of cerebellar granule progenitors. Allelic loss of chromosome 17p has also been described as the most frequent genetic defect in this human neoplasia. This observation raises the question of a possible interplay between 17p deletion and the Hedgehog tumorigenic pathway. Here, we identify the human orthologue of mouse [REN.sup.KCTD11], previously reported to be expressed in differentiating and low proliferating neuroblasts. Human [REN.sup.KCTD11] maps to 17p13.2 and displays allelic deletion as well as significantly reduced expression in medulloblastoma. [REN.sup.KCTD11] inhibits medulloblastoma cell proliferation and colony formation in vitro and suppresses xenograft tumor growth in vivo. [REN.sup.KCTD11] seems to inhibit medulloblastoma growth by negatively regulating the Hedgehog pathway because it antagonizes the Gli-mediated transactivation of Hedgehog target genes, by affecting Gill nuclear transfer, and its growth inhibitory activity is impaired by Gli1 inactivation. Therefore, we identify [REN.sup.KCTD11] as a suppressor of Hedgehog signaling and suggest that its inactivation might lead to a deregulation of the tumor-promoting Hedgehog pathway in medulloblastoma.

Published
2004

36. A homozygous MED11 C-terminal variant causes a lethal neurodegenerative disease

Author

Calì, Elisa, Lin, Sheng-Jia, Rocca, Clarissa, Sahin, Yavuz, Al Shamsi, Aisha, El Chehadeh, Salima, Chaabouni, Myriam, Mankad, Kshitij, Galanaki, Evangelia, Efthymiou, Stephanie, Sudhakar, Sniya, Athanasiou-Fragkouli, Alkyoni, Çelik, Tamer, Narlı, Nejat, Bianca, Sebastiano, Murphy, David, De Carvalho Moreira, Francisco Martins, Hannah, Michael G., Bugiardini, Enrico, Kriouile, Yamna, El Khorassani, Mohamed, Aguennouz, Mhammed, Groppa, Stanislav, Karashova, Blagovesta Marinova, Di Rosa, Gabriella, Goraya, Jatinder S., Sultan, Tipu, Avdjieva, Daniela, Kathom, Hadil, Tincheva, Radka, Banu, Selina, Veggiotti, Pierangelo, Verrotti, Alberto, Savasta, Salvatore, Ruiz, Alfons Macaya, Garavaglia, Barbara, Borgione, Eugenia, Papacostas, Savvas, Compagnoni, Chiara, Piccirilli, Alessandra, Vikelis, Michail, Chelban, Viorica, Kaiyrzhanov, Rauan, Cortese, Andrea, Sullivan, Roisin, Papanicolaou, Eleni Zamba, Dardiotis, Efthymios, Maqbool, Shazia, Ibrahim, Shahnaz, Kirmani, Salman, Rana, Nuzhat Noureen, Atawneh, Osama, Lim, Shen-Yang, Shaikh, Farooq, Scardamaglia, Annarita, Koutsis, George, Mangano, Salvatore, Scuderi, Carmela, Borgione, Eugenia, Morello, Giovanna, Zollo, Massimo, Heimer, Gali, Striano, Pasquale, Al-Khawaja, Issam, Al-Mutairi, Fuad, Alkuraya, Fowzan S., Rizig, Mie, Shashkin, Chingiz, Zharkynbekova, Nazira, Koneyev, Kairgali, Manizha, Ganieva, Isrofilov, Maksud, Guliyeva, Ulviyya, Salayev, Kamran, Khachatryan, Samson, Xiromerisiou, Georgia, Spanaki, Cleanthe, Tucci, Arianna, Fiorillo, Chiara, Rissotto, Federico, Munell, Francina, Gagliano, Antonella, Jan, Farida, Chimenz, Roberto, Gitto, Eloisa, Cuppari, Caterina, Romeo, Carmelo, Magrinelli, Francesca, Gupta, Neerja, Kabra, Madhulika, Benrhouma, Hanene, Tazir, Meriem, Zagaroli, Luca, Caloisi, Claudia, Fabiano, Cecilia, Bottone, Gabriella, Farello, Giovanni, Di Fabio, Sandra, Obeid, Makram, Bakhtadze, Sophia, Saadi, Nebal W., Zaki, Maha S., Triki, Chahnez C., Kara, Majdi, Belcastro, Vincenzo, Specchio, Nicola, Karimiani, Ehsan G., Salih, Ahmed M., Ramenghi, Luca A., David, Emanuele, Curró, Riccardo, Iezzi, Maria Laura, Iapadre, Giulia, Nanni, Giuliana, Scorrano, Giovanna, Fiorile, Maria F., Brancati, Francesco, Di Falco, Giovanna, Mandarà, Luana, Barrano, Giuseppe, Elia, Maurizio, Terrone, Gaetano, Operto, Francesca F., Valenzise, Mariella, Della Rocca, Ylenia, Zazzeroni, Francesca, Alesse, Edoardo, Manti, Filippo, Galosi, Serena, Nardecchia, Francesca, Leuzzi, Vincenzo, Pironti, Erica, Amore, Greta, Ceravolo, Giorgia, Zafar, Faisal, Ullah, Ehsan, Afzal, Erum, Javed, Iram, Rahman, Fatima, Ahmed, Muhammad Mehboob, Parisi, Pasquale, Borgia, Paola, Mangano, Giuseppe D., Chiarelli, Francesco, Genomics, Queen Square, Accogli, Andrea, Petree, Cassidy, Huang, Kevin, Monastiri, Kamel, Edizadeh, Masoud, Nardello, Rosaria, Ognibene, Marzia, De Marco, Patrizia, Ruggieri, Martino, Zara, Federico, Striano, Pasquale, Şahin, Yavuz, Al-Gazali, Lihadh, Abi Warde, Marie Therese, Gerard, Benedicte, Zifarelli, Giovanni, Beetz, Christian, Fortuna, Sara, Soler, Miguel, Valente, Enza Maria, Varshney, Gaurav, Maroofian, Reza, Salpietro, Vincenzo, and Houlden, Henry

Abstract

The mediator (MED) multisubunit-complex modulates the activity of the transcriptional machinery, and genetic defects in different MED subunits (17, 20, 27) have been implicated in neurologic diseases. In this study, we identified a recurrent homozygous variant in MED11(c.325C>T; p.Arg109Ter) in 7 affected individuals from 5 unrelated families.

Published
2022
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37. Induction of gadd45β by NF-κB downregulates pro-apoptotic JNK signalling

Author

De Smaele, Enrico, Zazzeroni, Francesca, Papa, Salvatore, Nguyen, Dung U., Jin, Rongguan, Jones, Joy, Cong, Rong, and Franzoso, Guido

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Enrico De Smaele; Francesca Zazzeroni; Salvatore Papa; Dung U. Nguyen; Rongguan Jin; Joy Jones; Rong Cong; Guido Franzoso (corresponding author) In addition to coordinating immune and inflammatory responses, NF-κB/Rel [...]

Published
2001
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41. The tumor suppressor gene KCTD11REN is regulated by Sp1 and methylation and its expression is reduced in tumors

Author

Rinaldi Christian, Di Camillo Raffaello, Murgo Simona, Po Agnese, Capece Daria, Ciccocioppo Lucia, Zazzeroni Francesca, Mancarelli M Michela, Ferretti Elisabetta, Gulino Alberto, and Alesse Edoardo

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract A hallmark of several human cancers is loss of heterozygosity (LOH) of chromosome 17p13. The same chromosomal region is also frequently hypermethylated in cancer. Although loss of 17p13 has been often associated with p53 genetic alteration or Hypermethylated in Cancer 1 (HIC1) gene hypermethylation, other tumor suppressor genes (TSGs) located in this region have critical roles in tumorigenesis. A novel TSG mapping on human chromosome 17p13.2 is KCTD11REN (KCTD11). We have recently demonstrated that KCTD11 expression is frequently lost in human medulloblastoma (MB), in part by LOH and in part by uncharacterized epigenetic events. Using a panel of human 177 tumor samples and their normal matching samples representing 18 different types of cancer, we show here that the down-regulation of KCTD11 protein level is a specific and a diffusely common event in tumorigenesis. Additionally, in order to characterize the regulatory regions in KCTD11 promoter, we identified a CpG island and several Sp1 binding sites on this promoter, and demonstrated that Sp1 transcription factor and DNA methylation contribute, at least in part, to regulate KCTD11 expression. Our findings identify KCTD11 as a widely down-regulated gene in human cancers, and provide a basis to understand how its expression might be deregulated in tumor cells.

Published
2010
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42. Turning an old GADDget into a troublemaker

Author

Capece, Daria, primary, D’Andrea, Daniel, additional, Verzella, Daniela, additional, Tornatore, Laura, additional, Begalli, Federica, additional, Bennett, Jason, additional, Zazzeroni, Francesca, additional, and Franzoso, Guido, additional

Published
2018
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43. GADD45β Loss Ablates Innate Immunosuppression in Cancer

Author

Verzella, Daniela, primary, Bennett, Jason, additional, Fischietti, Mariafausta, additional, Thotakura, Anil K., additional, Recordati, Camilla, additional, Pasqualini, Fabio, additional, Capece, Daria, additional, Vecchiotti, Davide, additional, D'Andrea, Daniel, additional, Di Francesco, Barbara, additional, De Maglie, Marcella, additional, Begalli, Federica, additional, Tornatore, Laura, additional, Papa, Salvatore, additional, Lawrence, Toby, additional, Forbes, Stuart J., additional, Sica, Antonio, additional, Alesse, Edoardo, additional, Zazzeroni, Francesca, additional, and Franzoso, Guido, additional

Published
2018
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45. Additional file 1: Figure S1. of MicroRNA expression analysis in high fat diet-induced NAFLD-NASH-HCC progression: study on C57BL/6J mice

Author

Tessitore, Alessandra, Cicciarelli, Germana, Vecchio, Filippo Del, Gaggiano, Agata, Verzella, Daniela, Mariafausta Fischietti, Mastroiaco, Valentina, Vetuschi, Antonella, Sferra, Roberta, Barnabei, Remo, Capece, Daria, Zazzeroni, Francesca, and Alesse, Edoardo

Subjects
Quantitative Biology::Tissues and Organs, Mathematics::Category Theory, Astrophysics::Solar and Stellar Astrophysics, Astrophysics::Cosmology and Extragalactic Astrophysics, Quantitative Biology::Cell Behavior
Abstract

Inflammatory infiltrate. Lymphocytes (green arrows), plasma cells (yellow arrows), macrophages (red arrows), and PMN (blue arrow). (PPTX 1448Â kb)

Published
2016
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46. Additional file 2: Figure S2. of MicroRNA expression analysis in high fat diet-induced NAFLD-NASH-HCC progression: study on C57BL/6J mice

Author

Tessitore, Alessandra, Cicciarelli, Germana, Vecchio, Filippo Del, Gaggiano, Agata, Verzella, Daniela, Mariafausta Fischietti, Mastroiaco, Valentina, Vetuschi, Antonella, Sferra, Roberta, Barnabei, Remo, Capece, Daria, Zazzeroni, Francesca, and Alesse, Edoardo

Abstract

MiRNAs differentially modulated during the progression of the hepatic damage. (A) RQ (relative quantification) values ± SE (Y axis) obtained by comparing HF to LF pooled RNAs from hepatic tissues. (B) RQ values ± SE (Y axis) of pooled RNAs from tumor tissues with respect to pooled RNAs from HF hepatic non-tumor tissues. Results are from 3 replicates. Global normalization mode was used for the analysis. Samples marked with the asterisk show P ≤ 0.05. (PDF 284 kb)

Published
2016
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47. Development of hepatocellular cancer induced by long term low fat-high carbohydrate diet in a NAFLD/NASH mouse model

Author

Tessitore, Alessandra, primary, Mastroiaco, Valentina, additional, Vetuschi, Antonella, additional, Sferra, Roberta, additional, Pompili, Simona, additional, Cicciarelli, Germana, additional, Barnabei, Remo, additional, Capece, Daria, additional, Zazzeroni, Francesca, additional, Capalbo, Carlo, additional, and Alesse, Edoardo, additional

Published
2017
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48. Ferritin heavy chain upregulation by NF-KappaB inhibits TNF alpha-induced apoptosis by suppressing reactive oxygen species

Author

Can G. Pham, Bubici, Concetta, Zazzeroni, Francesca, Jones, Joy, Papa, Salvatore, Alvarez, Kellean, Jayawardena, Shanthi, De Smaele, Enrico, Beaumont, Carole, Rong Cong, Torti, Frank M., Franzoso, Guido, and Torti, Suzy V.

Subjects
Tumor necrosis factor -- Research, Genetic transcription -- Research, Genetic research, Biological sciences
Abstract

A ferritin heavy chain (FHC), the primary iron storage factor, is identified in a study as an essential mediator of the antioxidant and protective activities of NF-KappaB. The antiapoptotic activity of FHC functions to inhibit induction of reactive oxygen species (ROS) and, thereby, activation of c-Jun N-terminal kinase (JNK) by tumor necrosis factor (TNF)alpha.

Published
2004

49. Additional file 2: Table S2. of Bioinformatics approach to predict target genes for dysregulated microRNAs in hepatocellular carcinoma: study on a chemically-induced HCC mouse model

Author

Vecchio, Filippo Del, Gallo, Francesco, Antinisca Di Marco, Mastroiaco, Valentina, Caianiello, Pasquale, Zazzeroni, Francesca, Alesse, Edoardo, and Tessitore, Alessandra

Abstract

The group of fifteen top target genes inferred from target prediction analysis. A table comprising the fifteen top target genes for the miR 125a-5p, miR-193b, miR-182 and miR-27a, retrieved from at least 50 % of prediction softwares used. (DOCX 11 kb)

Published
2015
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50. MicroRNAs in the DNA Damage/Repair Network and Cancer

Author

Tessitore, Alessandra, Cicciarelli, Germana, Del Vecchio, Filippo, Gaggiano, Agata, Verzella, Daniela, Fischietti, Mariafausta, Vecchiotti, Davide, Capece, Daria, Zazzeroni, Francesca, and Alesse, Edoardo

Subjects
Article Subject
Abstract

Cancer is a multistep process characterized by various and different genetic lesions which cause the transformation of normal cells into tumor cells. To preserve the genomic integrity, eukaryotic cells need a complex DNA damage/repair response network of signaling pathways, involving many proteins, able to induce cell cycle arrest, apoptosis, or DNA repair. Chemotherapy and/or radiation therapy are the most commonly used therapeutic approaches to manage cancer and act mainly through the induction of DNA damage. Impairment in the DNA repair proteins, which physiologically protect cells from persistent DNA injury, can affect the efficacy of cancer therapies. Recently, increasing evidence has suggested that microRNAs take actively part in the regulation of the DNA damage/repair network. MicroRNAs are endogenous short noncoding molecules able to regulate gene expression at the post-transcriptional level. Due to their activity, microRNAs play a role in many fundamental physiological and pathological processes. In this review we report and discuss the role of microRNAs in the DNA damage/repair and cancer.

Published
2014
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