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Article ; Online: Extracellular Flux Analysis to Investigate the Impact of NF-κB on Mitochondrial Respiration in Colorectal Carcinoma (CRC).

Capece, Daria / Verzella, Daniela / Begalli, Federica / Bennett, Jason / D'Andrea, Daniel / Vecchiotti, Davide / Zazzeroni, Francesca / Franzoso, Guido

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2366, Page(s) 293–303

Abstract: The reprogramming of cell metabolism is a hallmark of cancer. NF-κB transcription factors coordinate the host defense responses to stress, injury, and infection. They also play a central role in oncogenesis, at least in part by regulating cell metabolism ...

Abstract	The reprogramming of cell metabolism is a hallmark of cancer. NF-κB transcription factors coordinate the host defense responses to stress, injury, and infection. They also play a central role in oncogenesis, at least in part by regulating cell metabolism and the adaptation to energy stress conditions in various types of cancer, such as colorectal carcinoma (CRC). Here, we describe the XF Cell Mito Stress Test methodology aimed at characterizing the metabolic and bioenergetic profile of CRC cells following the silencing of the essential NF-κB subunit, RelA. This methodology may also be applied to other cancers to reveal novel core vulnerabilities of malignant cells.
MeSH term(s)	Colorectal Neoplasms/metabolism ; Energy Metabolism ; Humans ; Mitochondria/metabolism ; NF-kappa B/metabolism ; Respiration ; Transcription Factor RelA/genetics ; Transcription Factor RelA/metabolism
Chemical Substances	NF-kappa B ; Transcription Factor RelA
Language	English
Publishing date	2021-07-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1669-7_18
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Reprogramming immunosuppressive tumour-associated dendritic cells with GADD45β inhibitors.

Rajpoot, Sultan / Bennett, Jason / Franzoso, Guido / Verzella, Daniela / Begalli, Federica / Capece, Daria / D'Andrea, Daniel

Clinical medicine (London, England)

2020 Volume 20, Issue Suppl 2, Page(s) s116

MeSH term(s)	Dendritic Cells ; Humans ; Neoplasms
Language	English
Publishing date	2020-05-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2048646-7
ISSN	1473-4893 ; 1470-2118
ISSN (online)	1473-4893
ISSN	1470-2118
DOI	10.7861/clinmed.20-2-s116
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Article ; Online: Turning an old GADDget into a troublemaker.

Capece, Daria / D'Andrea, Daniel / Verzella, Daniela / Tornatore, Laura / Begalli, Federica / Bennett, Jason / Zazzeroni, Francesca / Franzoso, Guido

Cell death and differentiation

2018 Volume 25, Issue 4, Page(s) 642–644

MeSH term(s)	Animals ; Apoptosis/immunology ; Caspases/immunology ; Cytokines/immunology ; Humans ; Inflammation/immunology ; Inflammation/pathology ; NF-kappa B/immunology
Chemical Substances	Cytokines ; NF-kappa B ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2018-03-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-018-0087-6
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Zs.A 4230: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Unlocking the NF-κB Conundrum: Embracing Complexity to Achieve Specificity.

Begalli, Federica / Bennett, Jason / Capece, Daria / Verzella, Daniela / D'Andrea, Daniel / Tornatore, Laura / Franzoso, Guido

Biomedicines

2017 Volume 5, Issue 3

Abstract: Transcription factors of the nuclear factor κB (NF-κB) family are central coordinating regulators of the host defence responses to stress, injury and infection. Aberrant NF-κB activation also contributes to the pathogenesis of some of the most common ... ...

Abstract	Transcription factors of the nuclear factor κB (NF-κB) family are central coordinating regulators of the host defence responses to stress, injury and infection. Aberrant NF-κB activation also contributes to the pathogenesis of some of the most common current threats to global human health, including chronic inflammatory diseases, autoimmune disorders, diabetes, vascular diseases and the majority of cancers. Accordingly, the NF-κB pathway is widely considered an attractive therapeutic target in a broad range of malignant and non-malignant diseases. Yet, despite the aggressive efforts by the pharmaceutical industry to develop a specific NF-κB inhibitor, none has been clinically approved, due to the dose-limiting toxicities associated with the global suppression of NF-κB. In this review, we summarise the main strategies historically adopted to therapeutically target the NF-κB pathway with an emphasis on oncology, and some of the emerging strategies and newer agents being developed to pharmacologically inhibit this pathway.
Language	English
Publishing date	2017-08-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines5030050
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Article ; Online: NF-κB in the crosshairs: Rethinking an old riddle.

Bennett, Jason / Capece, Daria / Begalli, Federica / Verzella, Daniela / D'Andrea, Daniel / Tornatore, Laura / Franzoso, Guido

The international journal of biochemistry & cell biology

2017 Volume 95, Page(s) 108–112

Abstract: Constitutive NF-κB signalling has been implicated in the pathogenesis of most human malignancies and virtually all non-malignant pathologies. Accordingly, the NF-κB pathway has been aggressively pursued as an attractive therapeutic target for drug ... ...

Abstract	Constitutive NF-κB signalling has been implicated in the pathogenesis of most human malignancies and virtually all non-malignant pathologies. Accordingly, the NF-κB pathway has been aggressively pursued as an attractive therapeutic target for drug discovery. However, the severe on-target toxicities associated with systemic NF-κB inhibition have thus far precluded the development of a clinically useful, NF-κB-targeting medicine as a way to treat patients with either oncological or non-oncological diseases. This minireview discusses some of the more promising approaches currently being developed to circumvent the preclusive safety liabilities of global NF-κB blockade by selectively targeting pathogenic NF-κB signalling in cancer, while preserving the multiple physiological functions of NF-κB in host defence responses and tissue homeostasis.
MeSH term(s)	Animals ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Cell Survival/drug effects ; Drug Design ; Drugs, Investigational/adverse effects ; Drugs, Investigational/chemistry ; Drugs, Investigational/pharmacology ; Drugs, Investigational/therapeutic use ; Humans ; Models, Biological ; Molecular Targeted Therapy/adverse effects ; Molecular Targeted Therapy/trends ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/metabolism ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents ; Drugs, Investigational ; NF-kappa B ; Neoplasm Proteins
Language	English
Publishing date	2017-12-23
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2017.12.020
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Article ; Online: Unlocking the NF-κB Conundrum

Federica Begalli / Jason Bennett / Daria Capece / Daniela Verzella / Daniel D’Andrea / Laura Tornatore / Guido Franzoso

Biomedicines, Vol 5, Iss 3, p

Embracing Complexity to Achieve Specificity

2017 Volume 50

Abstract	Transcription factors of the nuclear factor κB (NF-κB) family are central coordinating regulators of the host defence responses to stress, injury and infection. Aberrant NF-κB activation also contributes to the pathogenesis of some of the most common current threats to global human health, including chronic inflammatory diseases, autoimmune disorders, diabetes, vascular diseases and the majority of cancers. Accordingly, the NF-κB pathway is widely considered an attractive therapeutic target in a broad range of malignant and non-malignant diseases. Yet, despite the aggressive efforts by the pharmaceutical industry to develop a specific NF-κB inhibitor, none has been clinically approved, due to the dose-limiting toxicities associated with the global suppression of NF-κB. In this review, we summarise the main strategies historically adopted to therapeutically target the NF-κB pathway with an emphasis on oncology, and some of the emerging strategies and newer agents being developed to pharmacologically inhibit this pathway.
Keywords	nuclear factor κB ; NF-κB inhibitors ; cancer ; IκB kinase ; Gadd45β ; ubiquitin ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2017-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: β

Po, Agnese / Begalli, Federica / Abballe, Luana / Alfano, Vincenzo / Besharat, Zein Mersini / Catanzaro, Giuseppina / Vacca, Alessandra / Napolitano, Maddalena / Tafani, Marco / Giangaspero, Felice / Locatelli, Franco / Ferretti, Elisabetta / Miele, Evelina

Stem cells international

2017 Volume 2017, Page(s) 5274171

Abstract: Cell development is regulated by a complex network of mRNA-encoded proteins and microRNAs, all funnelling onto the modulation of self-renewal or differentiation genes. How intragenic microRNAs and their host genes are transcriptionally coregulated and ... ...

Abstract	Cell development is regulated by a complex network of mRNA-encoded proteins and microRNAs, all funnelling onto the modulation of self-renewal or differentiation genes. How intragenic microRNAs and their host genes are transcriptionally coregulated and their functional relationships for the control of neural stem cells (NSCs) are poorly understood. We propose here the intragenic miR-326 and its host gene
Language	English
Publishing date	2017-02-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573856-2
ISSN	1687-9678 ; 1687-966X
ISSN (online)	1687-9678
ISSN	1687-966X
DOI	10.1155/2017/5274171
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Article ; Online: Enhanced triacylglycerol catabolism by carboxylesterase 1 promotes aggressive colorectal carcinoma.

Capece, Daria / D'Andrea, Daniel / Begalli, Federica / Goracci, Laura / Tornatore, Laura / Alexander, James L / Di Veroli, Alessandra / Leow, Shi-Chi / Vaiyapuri, Thamil S / Ellis, James K / Verzella, Daniela / Bennett, Jason / Savino, Luca / Ma, Yue / McKenzie, James S / Doria, Maria Luisa / Mason, Sam E / Chng, Kern Rei / Keun, Hector C /

Frost, Gary / Tergaonkar, Vinay / Broniowska, Katarzyna / Stunkel, Walter / Takats, Zoltan / Kinross, James M / Cruciani, Gabriele / Franzoso, Guido

The Journal of clinical investigation

2021 Volume 131, Issue 11

Abstract: The ability to adapt to low-nutrient microenvironments is essential for tumor cell survival and progression in solid cancers, such as colorectal carcinoma (CRC). Signaling by the NF-κB transcription factor pathway associates with advanced disease stages ... ...

Abstract	The ability to adapt to low-nutrient microenvironments is essential for tumor cell survival and progression in solid cancers, such as colorectal carcinoma (CRC). Signaling by the NF-κB transcription factor pathway associates with advanced disease stages and shorter survival in patients with CRC. NF-κB has been shown to drive tumor-promoting inflammation, cancer cell survival, and intestinal epithelial cell (IEC) dedifferentiation in mouse models of CRC. However, whether NF-κB affects the metabolic adaptations that fuel aggressive disease in patients with CRC is unknown. Here, we identified carboxylesterase 1 (CES1) as an essential NF-κB-regulated lipase linking obesity-associated inflammation with fat metabolism and adaptation to energy stress in aggressive CRC. CES1 promoted CRC cell survival via cell-autonomous mechanisms that fuel fatty acid oxidation (FAO) and prevent the toxic build-up of triacylglycerols. We found that elevated CES1 expression correlated with worse outcomes in overweight patients with CRC. Accordingly, NF-κB drove CES1 expression in CRC consensus molecular subtype 4 (CMS4), which is associated with obesity, stemness, and inflammation. CES1 was also upregulated by gene amplifications of its transcriptional regulator HNF4A in CMS2 tumors, reinforcing its clinical relevance as a driver of CRC. This subtype-based distribution and unfavorable prognostic correlation distinguished CES1 from other intracellular triacylglycerol lipases and suggest CES1 could provide a route to treat aggressive CRC.
MeSH term(s)	Carboxylic Ester Hydrolases/genetics ; Carboxylic Ester Hydrolases/metabolism ; Colorectal Neoplasms/enzymology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Female ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Triglycerides/genetics ; Triglycerides/metabolism
Chemical Substances	Neoplasm Proteins ; Triglycerides ; Carboxylic Ester Hydrolases (EC 3.1.1.-) ; CES1 protein, human (EC 3.1.1.1)
Language	English
Publishing date	2021-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI137845
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Article ; Online: β-Arrestin1/miR-326 Transcription Unit Is Epigenetically Regulated in Neural Stem Cells Where It Controls Stemness and Growth Arrest

Agnese Po / Federica Begalli / Luana Abballe / Vincenzo Alfano / Zein Mersini Besharat / Giuseppina Catanzaro / Alessandra Vacca / Maddalena Napolitano / Marco Tafani / Felice Giangaspero / Franco Locatelli / Elisabetta Ferretti / Evelina Miele

Stem Cells International, Vol

2017 Volume 2017

Abstract	Cell development is regulated by a complex network of mRNA-encoded proteins and microRNAs, all funnelling onto the modulation of self-renewal or differentiation genes. How intragenic microRNAs and their host genes are transcriptionally coregulated and their functional relationships for the control of neural stem cells (NSCs) are poorly understood. We propose here the intragenic miR-326 and its host gene β-arrestin1 as novel players whose epigenetic silencing maintains stemness in normal cerebellar stem cells. Such a regulation is mediated by CpG islands methylation of the common promoter. Epigenetic derepression of β-arrestin1/miR-326 by differentiation signals or demethylating agents leads to suppression of stemness features and cell growth and promotes cell differentiation. β-Arrestin1 inhibits cell proliferation by enhancing the nuclear expression of the cyclin-dependent kinase inhibitor p27. Therefore, we propose a new mechanism for the control of cerebellar NSCs where a coordinated epigenetic mechanism finely regulates β-arrestin1/miR-326 expression and consequently NSCs stemness and cell growth.
Keywords	Internal medicine ; RC31-1245
Subject code	571
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: β-arrestin1-mediated acetylation of Gli1 regulates Hedgehog/Gli signaling and modulates self-renewal of SHH medulloblastoma cancer stem cells.

Miele, Evelina / Po, Agnese / Begalli, Federica / Antonucci, Laura / Mastronuzzi, Angela / Marras, Carlo Efisio / Carai, Andrea / Cucchi, Danilo / Abballe, Luana / Besharat, Zein Mersini / Catanzaro, Giuseppina / Infante, Paola / Di Marcotullio, Lucia / Canettieri, Gianluca / De Smaele, Enrico / Screpanti, Isabella / Locatelli, Franco / Ferretti, Elisabetta

BMC cancer

2017 Volume 17, Issue 1, Page(s) 488

Abstract: Background: Aberrant Sonic Hedgehog/Gli (Hh/Gli) signaling pathway is a critical regulator of Sonic hedgehog medulloblastoma (SHH-MB). Cancer stem cells (CSCs), thought to be largely responsible for tumor initiation, maintenance, dissemination and ... ...

Abstract	Background: Aberrant Sonic Hedgehog/Gli (Hh/Gli) signaling pathway is a critical regulator of Sonic hedgehog medulloblastoma (SHH-MB). Cancer stem cells (CSCs), thought to be largely responsible for tumor initiation, maintenance, dissemination and relapse, have been identified in SHH-MB. Since we previously demonstrated that Hh/Gli signaling controls CSCs features in SHH-MB and that in these tumors miR-326 is down regulated, here we investigated whether there is a functional link between Hh/Gli signaling and miR-326. Methods: We evaluated β-arrestin1 (Arrb1) and its intragenic miR-326 levels in CSCs derived from SHH-MB. Subsequently, we modulated the expression of Arrb1 and miR-326 in CSCs in order to gain insight into their biological role. We also analyzed the mechanism by which Arrb1 and miR-326 control Hh/Gli signaling and self-renewal, using luciferase and protein immunoprecipitation assays. Results: Low levels of Arrb1 and miR-326 represent a feature of CSCs derived from SHH-MB. We observed that re-expression of Arrb1 and miR-326 inhibits Hh/Gli signaling pathway at multiple levels, which cause impaired proliferation and self-renewal, accompanied by down regulation of Nanog levels. In detail, miR-326 negatively regulates two components of the Hh/Gli pathway the receptor Smoothened (Smo) and the transcription factor Gli2, whereas Arrb1 suppresses the transcriptional activity of Gli1, by potentiating its p300-mediated acetylation. Conclusions: Our results identify a new molecular mechanism involving miR-326 and Arrb1 as regulators of SHH-MB CSCs. Specifically, low levels of Arrb1 and miR-326 trigger and maintain Hh/Gli signaling and self-renewal.
Language	English
Publishing date	2017-07-17
Publishing country	England
Document type	Journal Article
ISSN	1471-2407
ISSN (online)	1471-2407
DOI	10.1186/s12885-017-3477-0
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