Luca Parrillo

@cnr.it

CNR Researcher at IEOS - Istituto per l'Endocrinologia e l'Oncologia Sperimentale" Gaetano Salvatore" - Napoli
Consiglio Nazionale delle Ricerche (CNR)

Luca Parrillo


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https://researchid.co/lucpar80

RESEARCH, TEACHING, or OTHER INTERESTS

Biochemistry, Genetics and Molecular Biology, Molecular Medicine, Genetics, Aging
28

Scopus Publications

Scopus Publications

  • Distinctive chromosomal, mutational and transcriptional profiling in colon versus rectal cancers
    Maria Teresa De Angelis, Antonia Rizzuto, Angela Amaddeo, Carlo Sagnelli, Niccolò Vono, Michela Reda, Valentina Lise, Luca Parrillo, Carmela De Marco, Donatella Malanga, Gianluca Santamaria, Giuseppe Viglietto
    Journal of Translational Medicine, 2025
    BACKGROUND: Colorectal cancer (CRC) encompasses tumors arising in the colon (CC) and rectum (RC), often treated as a single disease despite emerging evidence of biological divergence. Understanding the molecular differences between CC and RC is critical for improving diagnosis, prognosis, and therapeutic strategies. METHODS: We performed an integrated genomic and transcriptomic analysis of CC and RC data from The Cancer Genome Atlas (TCGA) to investigate their degree of similarity and observed that these tumors present distinct molecular profiles, which suggest an evolution through divergent pathways. Comparative analyses included copy number alterations (CNAs), somatic mutations, driver gene prediction, differential gene expression, pathway enrichment, and survival analysis. RESULTS: Chromosomal analyses revealed that 43% of focal and 77% of large-scale CNAs were specific of CC, while 10.5% and 57% were specific of RC with 8% of mutant genes unique to CC and 0.18% to RC. CC and RC presented distinct profiles of gene mutations, with CC showing significantly higher tumor mutational burden (0.51 muts/Mb vs 0.28 muts/Mb in RC). Distinct mutational signatures were identified, with CC characterized by a higher frequency of PIK3CA, BRAF, and DNAH1 mutations, while RC showed enrichment for TP53 and NRAS mutations. Importantly, analysis of predicted non-canonical driver genes identified ACVR1B, LTBP4, SETD1A as CC-specific drivers and C4BPA, EHD1 as RC-specific drivers, underscoring divergent oncogenic mechanisms. However, the most substantial divergence was observed in transcriptomic profiling, with 56% and 33% of DEGs (in CC and RC, respectively) that were tumor-type specific. Notably, RC tumors segregated into two distinct transcriptional subtypes (Cluster 1 and Cluster 2), with Cluster 1 showed a more heterogeneous Consensus Molecular Subtypes (CMS) distribution, while Cluster 2 enriched in CMS4 (mesenchymal) and CMS3 (metabolic) consensus molecular subtypes. Accordingly, Gene Set Enrichment Analysis revealed CC-specific upregulation of Wnt, MYC, and mTOR signaling pathways, and RC-specific enrichment of GPCR and neuronal development pathways. On the other hand, pseudogene expression was significantly higher in CC, suggesting differential mechanisms of transcriptional dysregulation. Finally, we identified an RC-specific multigene survival signature as a prognostic model involving upregulation of C2CD4B, HSPD1P1, LINC01356, CBX3P9, GATA2-AS1 and downregulation of ATP5F1EP2, HSP90AB3P and SNRPFP1. CONCLUSIONS: Collectively, our findings provide robust molecular evidence that CC and RC follow divergent oncogenic pathways, emphasizing the need for site-specific biomarker development and therapeutic targeting in colorectal cancer.
  • Hypomethylation at PANDAR promoter progressively induces senescence in adipocyte precursor cells in subjects with obesity and type 2 diabetes
    Antonella Desiderio, Monica Pastorino, Michele Campitelli, Immacolata Prevenzano, Fatima Domenica Elisa De Palma, Rosa Spinelli, Luca Parrillo, Michele Longo, Marco Milone, Claudia Miele, Gregory Alexander Raciti, Francesco Beguinot
    FASEB Journal, 2024
    The risk of developing type 2 diabetes (T2D) is heterogeneous among individuals with obesity. Functional decline of adipocyte precursor cells (APCs) and accumulation of senescent cells in the subcutaneous adipose tissue contributes to the progression toward T2D. LncRNAs regulate cell senescence and may be implicated in determining this abnormality in APCs. Here, we report that APCs from individuals with obesity show a gradual increase in multiple senescence markers, which worsens in parallel with the progression from normal glucose tolerance (NGT) to impaired glucose tolerance (IGT) or T2D. Transcriptomic analysis identified PANDAR as the top‐ranked lncRNA differentially expressed in APCs from individuals with obesity and T2D and non‐obese subjects. Q‐PCR confirmed PANDAR up‐regulation in APCs from individuals with obesity, at progressively increased levels in those who developed, respectively, IGT and T2D. Bisulfite sequencing and luciferase assays revealed that, in parallel with glucose tolerance deterioration, the −1317 CpG at the PANDAR promoter became hypo‐methylated in obesity, resulting in enhanced PANDAR induction by p53. PANDAR silencing in senescent APCs from individuals with obesity and T2D caused repression of senescence programs and cell cycle re‐entry. PANDAR transcription in white blood cells (WBCs) mirrored that in APCs. Also, individuals with obesity exhibited rescue of PANDAR transcription in WBCs following bariatric surgery, accompanied by enhanced methylation at the regulatory PANDAR −1317 CpG. In conclusion, PANDAR dysregulation is a newly identified mechanism determining the early senescence of APCs from individuals with obesity, which worsens along the progression toward T2D. In the future, PANDAR targeting may represent a valuable strategy to delay this progression.
  • Altered H3K4me3 profile at the TFAM promoter causes mitochondrial alterations in preadipocytes from first-degree relatives of type 2 diabetics
    Michele Longo, Federica Zatterale, Rosa Spinelli, Jamal Naderi, Luca Parrillo, Pasqualina Florese, Cecilia Nigro, Alessia Leone, Augusta Moccia, Antonella Desiderio, Gregory A. Raciti, Claudia Miele, Ulf Smith, Francesco Beguinot
    Clinical Epigenetics, 2023
    Background First-degree relatives of type 2 diabetics (FDR) exhibit a high risk of developing type 2 diabetes (T2D) and feature subcutaneous adipocyte hypertrophy, independent of obesity. In FDR, adipose cell abnormalities contribute to early insulin-resistance and are determined by adipocyte precursor cells (APCs) early senescence and impaired recruitment into the adipogenic pathway. Epigenetic mechanisms signal adipocyte differentiation, leading us to hypothesize that abnormal epigenetic modifications cause adipocyte dysfunction and enhance T2D risk. To test this hypothesis, we examined the genome-wide histone profile in APCs from the subcutaneous adipose tissue of healthy FDR. Results Sequencing-data analysis revealed 2644 regions differentially enriched in lysine 4 tri-methylated H3-histone (H3K4me3) in FDR compared to controls (CTRL) with significant enrichment in mitochondrial-related genes. These included TFAM, which regulates mitochondrial DNA (mtDNA) content and stability. In FDR APCs, a significant reduction in H3K4me3 abundance at the TFAM promoter was accompanied by a reduction in TFAM mRNA and protein levels. FDR APCs also exhibited reduced mtDNA content and mitochondrial-genome transcription. In parallel, FDR APCs exhibited impaired differentiation and TFAM induction during adipogenesis. In CTRL APCs, TFAM-siRNA reduced mtDNA content, mitochondrial transcription and adipocyte differentiation in parallel with upregulation of the CDKN1A and ZMAT3 senescence genes. Furthermore, TFAM-siRNA significantly expanded hydrogen peroxide (H2O2)-induced senescence, while H2O2 did not affect TFAM expression. Conclusions Histone modifications regulate APCs ability to differentiate in mature cells, at least in part by modulating TFAM expression and affecting mitochondrial function. Reduced H3K4me3 enrichment at the TFAM promoter renders human APCs senescent and dysfunctional, increasing T2D risk. Graphical abstract
  • The Transcription Factor HOXA5: Novel Insights into Metabolic Diseases and Adipose Tissue Dysfunction
    Luca Parrillo, Rosa Spinelli, Michele Longo, Federica Zatterale, Gianluca Santamaria, Alessia Leone, Michele Campitelli, Gregory Alexander Raciti, Francesco Beguinot
    Cells, 2023
    The transcription factor HOXA5, from the HOX gene family, has long been studied due to its critical role in physiological activities in normal cells, such as organ development and body patterning, and pathological activities in cancer cells. Nonetheless, recent evidence supports the hypothesis of a role for HOXA5 in metabolic diseases, particularly in obesity and type 2 diabetes (T2D). In line with the current opinion that adipocyte and adipose tissue (AT) dysfunction belong to the group of primary defects in obesity, linking this condition to an increased risk of insulin resistance (IR) and T2D, the HOXA5 gene has been shown to regulate adipocyte function and AT remodeling both in humans and mice. Epigenetics adds complexity to HOXA5 gene regulation in metabolic diseases. Indeed, epigenetic mechanisms, specifically DNA methylation, influence the dynamic HOXA5 expression profile. In human AT, the DNA methylation profile at the HOXA5 gene is associated with hypertrophic obesity and an increased risk of developing T2D. Thus, an inappropriate HOXA5 gene expression may be a mechanism causing or maintaining an impaired AT function in obesity and potentially linking obesity to its associated disorders. In this review, we integrate the current evidence about the involvement of HOXA5 in regulating AT function, as well as its association with the pathogenesis of obesity and T2D. We also summarize the current knowledge on the role of DNA methylation in controlling HOXA5 expression. Moreover, considering the susceptibility of epigenetic changes to reversal through targeted interventions, we discuss the potential therapeutic value of targeting HOXA5 DNA methylation changes in the treatment of metabolic diseases.
  • Epigenetic Reprogramming of the Inflammatory Response in Obesity and Type 2 Diabetes
    Federica Zatterale, Gregory Alexander Raciti, Immacolata Prevenzano, Alessia Leone, Michele Campitelli, Veronica De Rosa, Francesco Beguinot, Luca Parrillo
    Biomolecules, 2022
    For the past several decades, the prevalence of obesity and type 2 diabetes (T2D) has continued to rise on a global level. The risk contributing to this pandemic implicates both genetic and environmental factors, which are functionally integrated by epigenetic mechanisms. While these conditions are accompanied by major abnormalities in fuel metabolism, evidence indicates that altered immune cell functions also play an important role in shaping of obesity and T2D phenotypes. Interestingly, these events have been shown to be determined by epigenetic mechanisms. Consistently, recent epigenome-wide association studies have demonstrated that immune cells from obese and T2D individuals feature specific epigenetic profiles when compared to those from healthy subjects. In this work, we have reviewed recent literature reporting epigenetic changes affecting the immune cell phenotype and function in obesity and T2D. We will further discuss therapeutic strategies targeting epigenetic marks for treating obesity and T2D-associated inflammation.
  • ZMAT3 hypomethylation contributes to early senescence of preadipocytes from healthy first-degree relatives of type 2 diabetics
    Rosa Spinelli, Pasqualina Florese, Luca Parrillo, Federica Zatterale, Michele Longo, Vittoria D’Esposito, Antonella Desiderio, Annika Nerstedt, Birgit Gustafson, Pietro Formisano, Claudia Miele, Gregory Alexander Raciti, Raffaele Napoli, Ulf Smith, Francesco Beguinot
    Aging Cell, 2022
    Senescence of adipose precursor cells (APC) impairs adipogenesis, contributes to the age‐related subcutaneous adipose tissue (SAT) dysfunction, and increases risk of type 2 diabetes (T2D). First‐degree relatives of T2D individuals (FDR) feature restricted adipogenesis, reflecting the detrimental effects of APC senescence earlier in life and rendering FDR more vulnerable to T2D. Epigenetics may contribute to these abnormalities but the underlying mechanisms remain unclear. In previous methylome comparison in APC from FDR and individuals with no diabetes familiarity (CTRL), ZMAT3 emerged as one of the top‐ranked senescence‐related genes featuring hypomethylation in FDR and associated with T2D risk. Here, we investigated whether and how DNA methylation changes at ZMAT3 promote early APC senescence. APC from FDR individuals revealed increases in multiple senescence markers compared to CTRL. Senescence in these cells was accompanied by ZMAT3 hypomethylation, which caused ZMAT3 upregulation. Demethylation at this gene in CTRL APC led to increased ZMAT3 expression and premature senescence, which were reverted by ZMAT3 siRNA. Furthermore, ZMAT3 overexpression in APC determined senescence and activation of the p53/p21 pathway, as observed in FDR APC. Adipogenesis was also inhibited in ZMAT3‐overexpressing APC. In FDR APC, rescue of ZMAT3 methylation through senolytic exposure simultaneously downregulated ZMAT3 expression and improved adipogenesis. Interestingly, in human SAT, aging and T2D were associated with significantly increased expression of both ZMAT3 and the P53 senescence marker. Thus, DNA hypomethylation causes ZMAT3 upregulation in FDR APC accompanied by acquisition of the senescence phenotype and impaired adipogenesis, which may contribute to FDR predisposition for T2D.
  • Epigenetic Dysregulation of the Homeobox A5 (HOXA5) Gene Associates with Subcutaneous Adipocyte Hypertrophy in Human Obesity
    Luca Parrillo, Rosa Spinelli, Mattia Costanzo, Pasqualina Florese, Serena Cabaro, Antonella Desiderio, Immacolata Prevenzano, Gregory Alexander Raciti, Ulf Smith, Claudia Miele, Pietro Formisano, Raffaele Napoli, Francesco Beguinot
    Cells, 2022
    Along with insulin resistance and increased risk of type 2 diabetes (T2D), lean first-degree relatives of T2D subjects (FDR) feature impaired adipogenesis in subcutaneous adipose tissue (SAT) and subcutaneous adipocyte hypertrophy well before diabetes onset. The molecular mechanisms linking these events have only partially been clarified. In the present report, we show that silencing of the transcription factor Homeobox A5 (HOXA5) in human preadipocytes impaired differentiation in mature adipose cells in vitro. The reduced adipogenesis was accompanied by inappropriate WNT-signaling activation. Importantly, in preadipocytes from FDR individuals, HOXA5 expression was attenuated, with hypermethylation of the HOXA5 promoter region found responsible for its downregulation, as revealed by luciferase assay. Both HOXA5 gene expression and DNA methylation were significantly correlated with SAT adipose cell hypertrophy in FDR, whose increased adipocyte size marks impaired adipogenesis. In preadipocytes from FDR, the low HOXA5 expression negatively correlated with enhanced transcription of the WNT signaling downstream genes NFATC1 and WNT2B. In silico evidence indicated that NFATC1 and WNT2B were directly controlled by HOXA5. The HOXA5 promoter region also was hypermethylated in peripheral blood leukocytes from these same FDR individuals, which was further revealed in peripheral blood leukocytes from an independent group of obese subjects. Thus, HOXA5 controlled adipogenesis in humans by suppressing WNT signaling. Altered DNA methylation of the HOXA5 promoter contributed to restricted adipogenesis in the SAT of lean subjects who were FDR of type 2 diabetics and in obese individuals.
  • Adipocyte precursor cells from first degree relatives of type 2 diabetic patients feature changes in hsa-mir-23a-5p, -193a-5p, and -193b-5p and insulin-like growth factor 2 expression
    Paola Mirra, Antonella Desiderio, Rosa Spinelli, Cecilia Nigro, Michele Longo, Luca Parrillo, Vittoria D’Esposito, Annamaria Carissimo, Shahram Hedjazifar, Ulf Smith, Pietro Formisano, Claudia Miele, Gregory A. Raciti, Francesco Beguinot
    FASEB Journal, 2021
    First‐degree relatives (FDRs) of type 2 diabetics (T2D) feature dysfunction of subcutaneous adipose tissue (SAT) long before T2D onset. miRNAs have a role in adipocyte precursor cells (APC) differentiation and in adipocyte identity. Thus, impaired miRNA expression may contribute to SAT dysfunction in FDRs. In the present work, we have explored changes in miRNA expression associated with T2D family history which may affect gene expression in SAT APCs from FDRs. Small RNA‐seq was performed in APCs from healthy FDRs and matched controls and omics data were validated by qPCR. Integrative analyses of APC miRNome and transcriptome from FDRs revealed down‐regulated hsa‐miR‐23a‐5p, ‐193a‐5p and ‐193b‐5p accompanied by up‐regulated Insulin‐like Growth Factor 2 (IGF2) gene which proved to be their direct target. The expression changes in these marks were associated with SAT adipocyte hypertrophy in FDRs. APCs from FDRs further demonstrated reduced capability to differentiate into adipocytes. Treatment with IGF2 protein decreased APC adipogenesis, while over‐expression of hsa‐miR‐23a‐5p, ‐193a‐5p and ‐193b‐5p enhanced adipogenesis by IGF2 targeting. Indeed, IGF2 increased the Wnt Family Member 10B gene expression in APCs. Down‐regulation of the three miRNAs and IGF2 up‐regulation was also observed in Peripheral Blood Leukocytes (PBLs) from FDRs. In conclusion, APCs from FDRs feature a specific miRNA/gene profile, which associates with SAT adipocyte hypertrophy and appears to contribute to impaired adipogenesis. PBL detection of this profile may help in identifying adipocyte hypertrophy in individuals at high risk of T2D.
  • Molecular basis of ageing in chronic metabolic diseases
    R. Spinelli, L. Parrillo, M. Longo, P. Florese, A. Desiderio, F. Zatterale, C. Miele, G. Alexander Raciti, F. Beguinot
    Journal of Endocrinological Investigation, 2020
    Aim Over the last decades, the shift in age distribution towards older ages and the progressive ageing which has occurred in most populations have been paralleled by a global epidemic of obesity and its related metabolic disorders, primarily, type 2 diabetes (T2D). Dysfunction of the adipose tissue (AT) is widely recognized as a significant hallmark of the ageing process that, in turn, results in systemic metabolic alterations. These include insulin resistance, accumulation of ectopic lipids and chronic inflammation, which are responsible for an elevated risk of obesity and T2D onset associated to ageing. On the other hand, obesity and T2D, the paradigms of AT dysfunction, share many physiological characteristics with the ageing process, such as an increased burden of senescent cells and epigenetic alterations. Thus, these chronic metabolic disorders may represent a state of accelerated ageing. Materials and methods A more precise explanation of the fundamental ageing mechanisms that occur in AT and a deeper understanding of their role in the interplay between accelerated ageing and AT dysfunction can be a fundamental leap towards novel therapies that address the causes, not just the symptoms, of obesity and T2D, utilizing strategies that target either senescent cells or DNA methylation. Results In this review, we summarize the current knowledge of the pathways that lead to AT dysfunction in the chronological ageing process as well as the pathophysiology of obesity and T2D, emphasizing the critical role of cellular senescence and DNA methylation. Conclusion Finally, we highlight the need for further research focused on targeting these mechanisms.
  • Altered PTPRD DNA methylation associates with restricted adipogenesis in healthy first-degree relatives of Type 2 diabetes subjects
    Luca Parrillo, Rosa Spinelli, Michele Longo, Antonella Desiderio, Paola Mirra, Cecilia Nigro, Francesca Fiory, Shahram Hedjazifar, Margherita Mutarelli, Annamaria Carissimo, Pietro Formisano, Claudia Miele, Ulf Smith, Gregory Alexander Raciti, Francesco Beguinot
    Epigenomics, 2020
    Aim: First-degree relatives (FDR) of individuals with Type 2 diabetes (T2D) feature restricted adipogenesis, which render them more vulnerable to T2D. Epigenetics may contribute to these abnormalities. Methods: FDR pre-adipocyte Methylome and Transcriptome were investigated by MeDIP- and RNA-Seq, respectively. Results: Methylome analysis revealed 2841 differentially methylated regions (DMR) in FDR. Most DMR localized into gene-body and were hypomethylated. The strongest hypomethylation signal was identified in an intronic-DMR at the PTPRD gene. PTPRD hypomethylation in FDR was confirmed by bisulphite sequencing and was responsible for its upregulation. Interestingly, Ptprd-overexpression in 3T3-L1 pre-adipocytes inhibited adipogenesis. Notably, the validated PTPRD-associated DMR was significantly hypomethylated in peripheral blood leukocytes from the same FDR individuals. Finally, PTPRD methylation pattern was also replicated in obese individuals. Conclusion: Our findings indicated a previously unrecognized role of PTPRD in restraining adipogenesis. This abnormality may contribute to increase FDR proclivity toward T2D.
  • Epigenetic silencing of the ANKRD26 gene correlates to the pro-inflammatory profile and increased cardio-metabolic risk factors in human obesity
    Antonella Desiderio, Michele Longo, Luca Parrillo, Michele Campitelli, Giuseppe Cacace, Sonia de Simone, Rosa Spinelli, Federica Zatterale, Serena Cabaro, Pasquale Dolce, Pietro Formisano, Marco Milone, Claudia Miele, Francesco Beguinot, Gregory A. Raciti
    Clinical Epigenetics, 2019
  • Nutritional factors, dna methylation, and risk of type 2 diabetes and obesity: Perspectives and challenges
    Luca Parrillo, Rosa Spinelli, Antonella Nicolò, Michele Longo, Paola Mirra, Gregory Alexander Raciti, Claudia Miele, Francesco Beguinot
    International Journal of Molecular Sciences, 2019
  • Adipose tissue dysfunction as determinant of obesity-associated metabolic complications
    Michele Longo, Federica Zatterale, Jamal Naderi, Luca Parrillo, Pietro Formisano, Gregory Alexander Raciti, Francesco Beguinot, Claudia Miele
    International Journal of Molecular Sciences, 2019
  • Methylglyoxal accumulation de-regulates HoxA5 expression, thereby impairing angiogenesis in glyoxalase 1 knock-down mouse aortic endothelial cells
    Cecilia Nigro, Alessia Leone, Michele Longo, Immacolata Prevenzano, Thomas H. Fleming, Antonella Nicolò, Luca Parrillo, Rosa Spinelli, Pietro Formisano, Peter P. Nawroth, Francesco Beguinot, Claudia Miele
    Biochimica Et Biophysica Acta Molecular Basis of Disease, 2019
  • Epigenetic modifications of the Zfp/ZNF423 gene control murine adipogenic commitment and are dysregulated in human hypertrophic obesity
    Michele Longo, Gregory A. Raciti, Federica Zatterale, Luca Parrillo, Antonella Desiderio, Rosa Spinelli, Ann Hammarstedt, Shahram Hedjazifar, Jenny M. Hoffmann, Cecilia Nigro, Paola Mirra, Francesca Fiory, Pietro Formisano, Claudia Miele, Ulf Smith, Francesco Beguinot
    Diabetologia, 2018
  • Targetting PED/PEA-15 for diabetes treatment
    Francesca Fiory, Rosa Spinelli, Gregory Alexander Raciti, Luca Parrillo, Vittoria D’esposito, Pietro Formisano, Claudia Miele, Francesco Beguinot
    Expert Opinion on Therapeutic Targets, 2017
  • Specific CpG hyper-methylation leads to Ankrd26 gene down-regulation in white adipose tissue of a mouse model of diet-induced obesity
    Gregory A. Raciti, Rosa Spinelli, Antonella Desiderio, Michele Longo, Luca Parrillo, Cecilia Nigro, Vittoria D’Esposito, Paola Mirra, Francesca Fiory, Vincenzo Pilone, Pietro Forestieri, Pietro Formisano, Ira Pastan, Claudia Miele, Francesco Beguinot
    Scientific Reports, 2017
  • Hoxa5 undergoes dynamic DNA methylation and transcriptional repression in the adipose tissue of mice exposed to high-fat diet
    L Parrillo, V Costa, G A Raciti, M Longo, R Spinelli, R Esposito, C Nigro, V Vastolo, A Desiderio, F Zatterale, A Ciccodicola, P Formisano, C Miele, F Beguinot
    International Journal of Obesity, 2016
  • Understanding type 2 diabetes: from genetics to epigenetics
    Gregory Alexander Raciti, Michele Longo, Luca Parrillo, Marco Ciccarelli, Paola Mirra, Paola Ungaro, Pietro Formisano, Claudia Miele, Francesco Béguinot
    Acta Diabetologica, 2015
  • Revising the embryonic origin of thyroid C cells in mice and humans
    Ellen Johansson, Louise Andersson, Jessica Örnros, Therese Carlsson, Camilla Ingeson-Carlsson, Shawn Liang, Jakob Dahlberg, Svante Jansson, Luca Parrillo, Pietro Zoppoli, Guillermo O. Barila, Daniel L. Altschuler, Daniela Padula, Heiko Lickert, Henrik Fagman, Mikael Nilsson
    Development Cambridge, 2015
  • PED/PEA-15 inhibits hydrogen peroxide-induced apoptosis in Ins-1E pancreatic beta-cells via PLD-1
    Francesca Fiory, Luca Parrillo, Gregory Alexander Raciti, Federica Zatterale, Cecilia Nigro, Paola Mirra, Roberta Falco, Luca Ulianich, Bruno Di Jeso, Pietro Formisano, Claudia Miele, Francesco Beguinot
    Plos One, 2014
  • Personalized medicine and type 2 diabetes: Lesson from epigenetics
    Gregory Alexander Raciti, Cecilia Nigro, Michele Longo, Luca Parrillo, Claudia Miele, Pietro Formisano, Francesco Béguinot
    Epigenomics, 2014
  • GRP78 mediates cell growth and invasiveness in endometrial cancer
    Gaetano Calì, Luigi Insabato, Domenico Conza, Giuseppe Bifulco, Luca Parrillo, Paola Mirra, Francesca Fiory, Claudia Miele, Gregory Alexander Raciti, Bruno Di Jeso, Giuseppe Terrazzano, Francesco Beguinot, Luca Ulianich
    Journal of Cellular Physiology, 2014
  • PREP1 deficiency downregulates hepatic lipogenesis and attenuates steatohepatitis in mice
    Francesco Oriente, Serena Cabaro, Antonietta Liotti, Michele Longo, Luca Parrillo, Teresa Bruna Pagano, Gregory Alexander Raciti, Dmitry Penkov, Orlando Paciello, Claudia Miele, Pietro Formisano, Francesco Blasi, Francesco Beguinot
    Diabetologia, 2013
  • An essential role for Pax8 in the transcriptional regulation of Cadherin-16 in thyroid cells
    Tiziana de Cristofaro, Tina Di Palma, Imma Fichera, Valeria Lucci, Luca Parrillo, Mario De Felice, Mariastella Zannini
    Molecular Endocrinology, 2012
  • Increased hexosamine biosynthetic pathway flux dedifferentiates INS-1E cells and murine islets by an extracellular signal-regulated kinase (ERK)1/2-mediated signal transmission pathway
    A. Lombardi, L. Ulianich, A. S. Treglia, C. Nigro, L. Parrillo, D. D. Lofrumento, G. Nicolardi, C. Garbi, F. Beguinot, C. Miele, B. Di Jeso
    Diabetologia, 2012
  • MSX1 and TGF-β3 are novel target genes functionally regulated by FOXE1
    I. Venza, M. Visalli, L. Parrillo, M. De Felice, D. Teti, M. Venza
    Human Molecular Genetics, 2011
  • Gene expression profiling at early organogenesis reveals both common and diverse mechanisms in foregut patterning
    Henrik Fagman, Elena Amendola, Luca Parrillo, Pietro Zoppoli, Pina Marotta, Marzia Scarfò, Pasquale De Luca, Denise Pires de Carvalho, Michele Ceccarelli, Mario De Felice, Roberto Di Lauro
    Developmental Biology, 2011