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Article ; Online: NK cell surveillance of hematological malignancies. Therapeutic implications and regulation by chemokine receptors.

Tomaipitinca, Luana / Russo, Eleonora / Bernardini, Giovanni

2021 Volume 80, Page(s) 100968

Abstract: NK cells are circulating innate lymphoid cells that constantly move from bloodstream into tissues, exerting several functions including tumor surveillance. For this reason, NK cells are considered attractive target for cancer immunotherapy. Several ... ...

Abstract	NK cells are circulating innate lymphoid cells that constantly move from bloodstream into tissues, exerting several functions including tumor surveillance. For this reason, NK cells are considered attractive target for cancer immunotherapy. Several strategies are employed to harness NK cell efficacy especially in hematological tumors, including adoptive transfer, genetic manipulation to overexpress chimeric antigen receptors and cytokine or immunomodulatory drug treatments of ex-vivo cultivated and expanded NK cells. Several chemokine receptors support NK cell tissue homing and are required for efficient tumor infiltration. Nevertheless, chemokine receptor expression is often insufficient, or their respective ligands may not be expressed in the tumor microenvironment, thus limiting NK cell localization at the tumor site. Therefore, strategies to implement expression or promote the function of the correct chemokine receptor/ligand axes have been employed in the last years with promising results in preclinical models. In this review, we discuss how chemokine receptors and their ligands regulate the trafficking and localization of NK cells in hematological tumors and how the chemokine function can be manipulated to improve current therapeutic approaches.
MeSH term(s)	Hematologic Neoplasms/therapy ; Humans ; Immunity, Innate ; Killer Cells, Natural ; Receptors, Chemokine/genetics ; Tumor Microenvironment
Chemical Substances	Receptors, Chemokine
Language	English
Publishing date	2021-05-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	197640-0
ISSN	1872-9452 ; 0098-2997
ISSN (online)	1872-9452
ISSN	0098-2997
DOI	10.1016/j.mam.2021.100968
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Article: Expression of Genes Related to Lipid Handling and the Obesity Paradox in Melanoma: Database Analysis.

Giampietri, Claudia / Tomaipitinca, Luana / Scatozza, Francesca / Facchiano, Antonio

JMIR cancer

2020 Volume 6, Issue 1, Page(s) e16974

Abstract: Background: Publicly available genomic and transcriptomic data in searchable databases allow researchers to investigate specific medical issues in thousands of patients. Many studies have highlighted the role lipids play in cancer initiation and ... ...

Abstract	Background: Publicly available genomic and transcriptomic data in searchable databases allow researchers to investigate specific medical issues in thousands of patients. Many studies have highlighted the role lipids play in cancer initiation and progression and reported nutritional interventions aimed at improving prognosis and survival. Therefore, there is an increasing interest in the role that fat intake may play in cancer. It is known that there is a relationship between BMI and survival in patients with cancer, and that there is an association between a high-fat diet and increased cancer risk. In some cancers, such as colorectal cancer, obesity and high fat intake are known to increase the risk of cancer initiation and progression. On the contrary, in patients undergoing treatment for melanoma, a higher BMI unexpectedly acts as a protective factor rather than a risk factor; this phenomenon is known as the obesity paradox. Objective: We aimed to identify the molecular mechanism underlying the obesity paradox, with the expectation that this could indicate new effective strategies to reduce risk factors and improve protective approaches. Methods: In order to determine the genes potentially involved in this process, we investigated the expression values of lipid-related genes in patients with melanoma or colorectal cancer. We used available data from 2990 patients from 3 public databases (IST [In Silico Transcriptomics] Online, GEO [Gene Expression Omnibus], and Oncomine) in an analysis that involved 3 consecutive validation steps. Of this group, data from 1410 individuals were analyzed in the IST Online database (208 patients with melanoma and 147 healthy controls, as well as 991 patients with colorectal cancer and 64 healthy controls). In addition, 45 melanoma, 18 nevi, and 7 healthy skin biopsies were analyzed in another database, GEO, to validate the IST Online data. Finally, using the Oncomine database, 318 patients with melanoma (312 controls) and 435 patients with colorectal cancer (445 controls) were analyzed. Results: In the first and second database investigated (IST Online and GEO, respectively), patients with melanoma consistently showed significantly (P<.001) lower expression levels of 4 genes compared to healthy controls: CD36, MARCO, FABP4, and FABP7. This strong reduction was not observed in patients with colorectal cancer. An additional analysis was carried out on a DNA-TCGA data set from the Oncomine database, further validating CD36 and FABP4. Conclusions: The observed lower expression of genes such as CD36 and FABP4 in melanoma may reduce the cellular internalization of fat and therefore make patients with melanoma less sensitive to a high dietary fat intake, explaining in part the obesity paradox observed in patients with melanoma.
Language	English
Publishing date	2020-05-19
Publishing country	Canada
Document type	Journal Article
ISSN	2369-1999
ISSN	2369-1999
DOI	10.2196/16974
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Article ; Online: Skin mesenchymal niches maintain and protect AML-initiating stem cells.

Sandhow, Lakshmi / Cai, Huan / Leonard, Elory / Xiao, Pingnan / Tomaipitinca, Luana / Månsson, Alma / Kondo, Makoto / Sun, Xiaoyan / Johansson, Anne-Sofie / Tryggvason, Karl / Kasper, Maria / Järås, Marcus / Qian, Hong

The Journal of experimental medicine

2023 Volume 220, Issue 10

Abstract: Leukemia cutis or leukemic cell infiltration in skin is one of the common extramedullary manifestations of acute myeloid leukemia (AML) and signifies a poorer prognosis. However, its pathogenesis and maintenance remain understudied. Here, we report ... ...

Abstract	Leukemia cutis or leukemic cell infiltration in skin is one of the common extramedullary manifestations of acute myeloid leukemia (AML) and signifies a poorer prognosis. However, its pathogenesis and maintenance remain understudied. Here, we report massive AML cell infiltration in the skin in a transplantation-induced MLL-AF9 AML mouse model. These AML cells could regenerate AML after transplantation. Prospective niche characterization revealed that skin harbored mesenchymal progenitor cells (MPCs) with a similar phenotype as BM mesenchymal stem cells. These skin MPCs protected AML-initiating stem cells (LSCs) from chemotherapy in vitro partially via mitochondrial transfer. Furthermore, Lama4 deletion in skin MPCs promoted AML LSC proliferation and chemoresistance. Importantly, more chemoresistant AML LSCs appeared to be retained in Lama4-/- mouse skin after cytarabine treatment. Our study reveals the characteristics and previously unrecognized roles of skin mesenchymal niches in maintaining and protecting AML LSCs during chemotherapy, meriting future exploration of their impact on AML relapse.
MeSH term(s)	Animals ; Mice ; Prospective Studies ; Stem Cells ; Skin ; Leukemia, Myeloid, Acute ; Mesenchymal Stem Cells
Language	English
Publishing date	2023-07-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20220953
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Article ; Online: NK Cell Anti-Tumor Surveillance in a Myeloid Cell-Shaped Environment.

Russo, Eleonora / Laffranchi, Mattia / Tomaipitinca, Luana / Del Prete, Annalisa / Santoni, Angela / Sozzani, Silvano / Bernardini, Giovanni

Frontiers in immunology

2021 Volume 12, Page(s) 787116

Abstract: NK cells are innate lymphoid cells endowed with cytotoxic capacity that play key roles in the immune surveillance of tumors. Increasing evidence indicates that NK cell anti-tumor response is shaped by bidirectional interactions with myeloid cell subsets ... ...

Abstract	NK cells are innate lymphoid cells endowed with cytotoxic capacity that play key roles in the immune surveillance of tumors. Increasing evidence indicates that NK cell anti-tumor response is shaped by bidirectional interactions with myeloid cell subsets such as dendritic cells (DCs) and macrophages. DC-NK cell crosstalk in the tumor microenvironment (TME) strongly impacts on the overall NK cell anti-tumor response as DCs can affect NK cell survival and optimal activation while, in turn, NK cells can stimulate DCs survival, maturation and tumor infiltration through the release of soluble factors. Similarly, macrophages can either shape NK cell differentiation and function by expressing activating receptor ligands and/or cytokines, or they can contribute to the establishment of an immune-suppressive microenvironment through the expression and secretion of molecules that ultimately lead to NK cell inhibition. Consequently, the exploitation of NK cell interaction with DCs or macrophages in the tumor context may result in an improvement of efficacy of immunotherapeutic approaches.
MeSH term(s)	Animals ; Cell Communication/immunology ; Cell Survival/immunology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Disease Models, Animal ; Humans ; Immunologic Surveillance ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Neoplasms/immunology ; Neoplasms/pathology ; Tumor Microenvironment/immunology
Language	English
Publishing date	2021-12-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.787116
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Article ; Online: The Role of Autophagy in Liver Epithelial Cells and Its Impact on Systemic Homeostasis.

Tomaipitinca, Luana / Mandatori, Sara / Mancinelli, Romina / Giulitti, Federico / Petrungaro, Simonetta / Moresi, Viviana / Facchiano, Antonio / Ziparo, Elio / Gaudio, Eugenio / Giampietri, Claudia

Nutrients

2019 Volume 11, Issue 4

Abstract: ...

Abstract	:
MeSH term(s)	Autophagy/physiology ; Bile Ducts/cytology ; Cell Death ; Diet ; Dyslipidemias ; Endothelial Cells/physiology ; Energy Intake ; Epithelial Cells/physiology ; Hepatocytes/physiology ; Homeostasis/physiology ; Humans ; Kupffer Cells/physiology ; Lipid Metabolism/physiology ; Lipolysis ; Liver/cytology ; Melanoma ; Muscle, Skeletal/metabolism ; Neoplasms ; Oxidative Stress
Language	English
Publishing date	2019-04-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu11040827
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Article ; Online: c-FLIP regulates autophagy by interacting with Beclin-1 and influencing its stability.

Tomaipitinca, Luana / Petrungaro, Simonetta / D'Acunzo, Pasquale / Facchiano, Angelo / Dubey, Amit / Rizza, Salvatore / Giulitti, Federico / Gaudio, Eugenio / Filippini, Antonio / Ziparo, Elio / Cecconi, Francesco / Giampietri, Claudia

Cell death & disease

2021 Volume 12, Issue 7, Page(s) 686

Abstract: c-FLIP (cellular FLICE-like inhibitory protein) protein is mostly known as an apoptosis modulator. However, increasing data underline that c-FLIP plays multiple roles in cellular homoeostasis, influencing differently the same pathways depending on its ... ...

Abstract	c-FLIP (cellular FLICE-like inhibitory protein) protein is mostly known as an apoptosis modulator. However, increasing data underline that c-FLIP plays multiple roles in cellular homoeostasis, influencing differently the same pathways depending on its expression level and isoform predominance. Few and controversial data are available regarding c-FLIP function in autophagy. Here we show that autophagic flux is less effective in c-FLIP-/- than in WT MEFs (mouse embryonic fibroblasts). Indeed, we show that the absence of c-FLIP compromises the expression levels of pivotal factors in the generation of autophagosomes. In line with the role of c-FLIP as a scaffold protein, we found that c-FLIP
Language	English
Publishing date	2021-07-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-021-03957-5
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Article: Anti-tumor Effect of Oleic Acid in Hepatocellular Carcinoma Cell Lines

Giulitti, Federico / Petrungaro, Simonetta / Mandatori, Sara / Tomaipitinca, Luana / de Franchis, Valerio / D'Amore, Antonella / Filippini, Antonio / Gaudio, Eugenio / Ziparo, Elio / Giampietri, Claudia

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 629182

Abstract: Oleic acid (OA) is a component of the olive oil. Beneficial health effects of olive oil are well-known, such as protection against liver steatosis and against some cancer types. In the present study, we focused on OA effects in hepatocellular carcinoma ( ... ...

Abstract	Oleic acid (OA) is a component of the olive oil. Beneficial health effects of olive oil are well-known, such as protection against liver steatosis and against some cancer types. In the present study, we focused on OA effects in hepatocellular carcinoma (HCC), investigating responses to OA treatment (50-300 μM) in HCC cell lines (Hep3B and Huh7.5) and in a healthy liver-derived human cell line (THLE-2). Upon OA administration higher lipid accumulation, perilipin-2 increase, and autophagy reduction were observed in HCC cells as compared to healthy cells. OA in the presence of 10% FBS significantly reduced viability of HCC cell lines at 300 μM through Alamar Blue staining evaluation, and reduced cyclin D1 expression in a dose-dependent manner while it was ineffective on healthy hepatocytes. Furthermore, OA increased cell death by about 30%, inducing apoptosis and necrosis in HCC cells but not in healthy hepatocytes at 300 μM dosage. Moreover, OA induced senescence in Hep3B, reduced P-ERK in both HCC cell lines and significantly inhibited the antiapoptotic proteins c-Flip and Bcl-2 in HCC cells but not in healthy hepatocytes. All these results led us to conclude that different cell death processes occur in these two HCC cell lines upon OA treatment. Furthermore, 300 μM OA significantly reduced the migration and invasion of both HCC cell lines, while it has no effects on healthy cells. Finally, we investigated autophagy role in OA-dependent effects by using the autophagy inducer torin-1. Combined OA/torin-1 treatment reduced lipid accumulation and cell death as compared to single OA treatment. We therefore concluded that OA effects in HCC cells lines are, at least, in part dependent on OA-induced autophagy reduction. In conclusion, we report for the first time an autophagy dependent relevant anti-cancer effect of OA in human hepatocellular carcinoma cell lines.
Language	English
Publishing date	2021-02-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.629182
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Article: The Role of Autophagy in Liver Epithelial Cells and Its Impact on Systemic Homeostasis

Tomaipitinca, Luana / Mandatori, Sara / Mancinelli, Romina / Giulitti, Federico / Petrungaro, Simonetta / Moresi, Viviana / Facchiano, Antonio / Ziparo, Elio / Gaudio, Eugenio / Giampietri, Claudia

Nutrients. 2019 Apr. 11, v. 11, no. 4

2019

Abstract: Autophagy plays a role in several physiological and pathological processes as it controls the turnover rate of cellular components and influences cellular homeostasis. The liver plays a central role in controlling organisms’ metabolism, regulating ... ...

Abstract	Autophagy plays a role in several physiological and pathological processes as it controls the turnover rate of cellular components and influences cellular homeostasis. The liver plays a central role in controlling organisms’ metabolism, regulating glucose storage, plasma proteins and bile synthesis and the removal of toxic substances. Liver functions are particularly sensitive to autophagy modulation. In this review we summarize studies investigating how autophagy influences the hepatic metabolism, focusing on fat accumulation and lipids turnover. We also describe how autophagy affects bile production and the scavenger function within the complex homeostasis of the liver. We underline the role of hepatic autophagy in counteracting the metabolic syndrome and the associated cardiovascular risk. Finally, we highlight recent reports demonstrating how the autophagy occurring within the liver may affect skeletal muscle homeostasis as well as different extrahepatic solid tumors, such as melanoma.
Keywords	autophagy ; bile ; blood proteins ; epithelial cells ; glucose ; homeostasis ; lipids ; liver ; melanoma ; metabolic syndrome ; metabolism ; skeletal muscle ; toxic substances
Language	English
Dates of publication	2019-0411
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu11040827
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Lipid Storage and Autophagy in Melanoma Cancer Cells.

Giampietri, Claudia / Petrungaro, Simonetta / Cordella, Martina / Tabolacci, Claudio / Tomaipitinca, Luana / Facchiano, Antonio / Eramo, Adriana / Filippini, Antonio / Facchiano, Francesco / Ziparo, Elio

International journal of molecular sciences

2017 Volume 18, Issue 6

Abstract: Cancer stem cells (CSC) represent a key cellular subpopulation controlling biological features such as cancer progression in all cancer types. By using melanospheres established from human melanoma patients, we compared less differentiated melanosphere- ... ...

Abstract	Cancer stem cells (CSC) represent a key cellular subpopulation controlling biological features such as cancer progression in all cancer types. By using melanospheres established from human melanoma patients, we compared less differentiated melanosphere-derived CSC to differentiating melanosphere-derived cells. Increased lipid uptake was found in melanosphere-derived CSC vs. differentiating melanosphere-derived cells, paralleled by strong expression of lipogenic factors Sterol Regulatory Element-Binding Protein-1 (SREBP-1) and Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ). An inverse relation between lipid-storing phenotype and autophagy was also found, since microtubule-associated protein 1A/1B-Light Chain 3 (LC3) lipidation is reduced in melanosphere-derived CSC. To investigate upstream autophagy regulators, Phospho-AMP activated Protein Kinase (P-AMPK) and Phospho-mammalian Target of Rapamycin (P-mTOR) were analyzed; lower P-AMPK and higher P-mTOR expression in melanosphere-derived CSC were found, thus explaining, at least in part, their lower autophagic activity. In addition, co-localization of LC3-stained autophagosome spots and perilipin-stained lipid droplets was demonstrated mainly in differentiating melanosphere-derived cells, further supporting the role of autophagy in lipid droplets clearance. The present manuscript demonstrates an inverse relationship between lipid-storing phenotype and melanoma stem cells differentiation, providing novel indications involving autophagy in melanoma stem cells biology.
Language	English
Publishing date	2017-06-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms18061271
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Article ; Online: Multifaceted Roles of GSK-3 in Cancer and Autophagy-Related Diseases.

Mancinelli, Romina / Carpino, Guido / Petrungaro, Simonetta / Mammola, Caterina Loredana / Tomaipitinca, Luana / Filippini, Antonio / Facchiano, Antonio / Ziparo, Elio / Giampietri, Claudia

Oxidative medicine and cellular longevity

2017 Volume 2017, Page(s) 4629495

Abstract: GSK-3 is a ubiquitously expressed serine/threonine kinase existing as GSK- ... ...

Abstract	GSK-3 is a ubiquitously expressed serine/threonine kinase existing as GSK-3
MeSH term(s)	Animals ; Apoptosis ; Autophagy ; Glycogen Synthase Kinase 3/genetics ; Glycogen Synthase Kinase 3/metabolism ; Glycogen Synthase Kinase 3 beta/genetics ; Glycogen Synthase Kinase 3 beta/metabolism ; Humans ; Liver Diseases/enzymology ; Liver Diseases/genetics ; Liver Diseases/pathology ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplasms/enzymology ; Neoplasms/genetics ; Neoplasms/pathology ; Neurodegenerative Diseases/enzymology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/pathology ; Oxidative Stress
Chemical Substances	Neoplasm Proteins ; GSK3B protein, human (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; glycogen synthase kinase 3 alpha (EC 2.7.11.26)
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2017/4629495
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