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Article ; Online: Breast cancers as ecosystems: a metabolic perspective.

Martino, Flavia / Lupi, Mariadomenica / Giraudo, Enrico / Lanzetti, Letizia

Cellular and molecular life sciences : CMLS

2023 Volume 80, Issue 9, Page(s) 244

Abstract: Breast cancer (BC) is the most frequently diagnosed cancer and one of the major causes of cancer death. Despite enormous progress in its management, both from the therapeutic and early diagnosis viewpoints, still around 700,000 patients succumb to the ... ...

Abstract	Breast cancer (BC) is the most frequently diagnosed cancer and one of the major causes of cancer death. Despite enormous progress in its management, both from the therapeutic and early diagnosis viewpoints, still around 700,000 patients succumb to the disease each year, worldwide. Late recurrency is the major problem in BC, with many patients developing distant metastases several years after the successful eradication of the primary tumor. This is linked to the phenomenon of metastatic dormancy, a still mysterious trait of the natural history of BC, and of several other types of cancer, by which metastatic cells remain dormant for long periods of time before becoming reactivated to initiate the clinical metastatic disease. In recent years, it has become clear that cancers are best understood if studied as ecosystems in which the impact of non-cancer-cell-autonomous events-dependent on complex interaction between the cancer and its environment, both local and systemic-plays a paramount role, probably as significant as the cell-autonomous alterations occurring in the cancer cell. In adopting this perspective, a metabolic vision of the cancer ecosystem is bound to improve our understanding of the natural history of cancer, across space and time. In BC, many metabolic pathways are coopted into the cancer ecosystem, to serve the anabolic and energy demands of the cancer. Their study is shedding new light on the most critical aspect of BC management, of metastatic dissemination, and that of the related phenomenon of dormancy and fostering the application of the knowledge to the development of metabolic therapies.
MeSH term(s)	Humans ; Female ; Breast Neoplasms/pathology ; Ecosystem
Language	English
Publishing date	2023-08-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-04902-9
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Article ; Online: A novel function of Rab5 in mitosis.

Lanzetti, Letizia

Small GTPases

2012 Volume 3, Issue 3, Page(s) 168–172

Abstract: Several membrane trafficking proteins have been shown to participate in spindle assembly and stability during mitosis. Despite the fact that the role of some of them has been clarified, the requirement for these molecules in mitosis is still poorly ... ...

Abstract	Several membrane trafficking proteins have been shown to participate in spindle assembly and stability during mitosis. Despite the fact that the role of some of them has been clarified, the requirement for these molecules in mitosis is still poorly understood.
MeSH term(s)	Animals ; Chromosomal Proteins, Non-Histone/analysis ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosomes/metabolism ; Humans ; Kinetochores/metabolism ; Microfilament Proteins/analysis ; Microfilament Proteins/metabolism ; Mitosis ; rab5 GTP-Binding Proteins/analysis ; rab5 GTP-Binding Proteins/metabolism
Chemical Substances	Chromosomal Proteins, Non-Histone ; Microfilament Proteins ; centromere protein F ; rab5 GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2012-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2682247-7
ISSN	2154-1256 ; 2154-1248
ISSN (online)	2154-1256
ISSN	2154-1248
DOI	10.4161/sgtp.19987
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Article ; Online: Endocytosis in the context-dependent regulation of individual and collective cell properties.

Sigismund, Sara / Lanzetti, Letizia / Scita, Giorgio / Di Fiore, Pier Paolo

Nature reviews. Molecular cell biology

2021 Volume 22, Issue 9, Page(s) 625–643

Abstract: Endocytosis allows cells to transport particles and molecules across the plasma membrane. In addition, it is involved in the termination of signalling through receptor downmodulation and degradation. This traditional outlook has been substantially ... ...

Abstract	Endocytosis allows cells to transport particles and molecules across the plasma membrane. In addition, it is involved in the termination of signalling through receptor downmodulation and degradation. This traditional outlook has been substantially modified in recent years by discoveries that endocytosis and subsequent trafficking routes have a profound impact on the positive regulation and propagation of signals, being key for the spatiotemporal regulation of signal transmission in cells. Accordingly, endocytosis and membrane trafficking regulate virtually every aspect of cell physiology and are frequently subverted in pathological conditions. Two key aspects of endocytic control over signalling are coming into focus: context-dependency and long-range effects. First, endocytic-regulated outputs are not stereotyped but heavily dependent on the cell-specific regulation of endocytic networks. Second, endocytic regulation has an impact not only on individual cells but also on the behaviour of cellular collectives. Herein, we will discuss recent advancements in these areas, highlighting how endocytic trafficking impacts complex cell properties, including cell polarity and collective cell migration, and the relevance of these mechanisms to disease, in particular cancer.
MeSH term(s)	Animals ; Biological Transport ; Cell Membrane/metabolism ; Cell Movement ; Cell Polarity ; Endocytosis/physiology ; Endosomes/metabolism ; Humans ; Morphogenesis ; Signal Transduction
Language	English
Publishing date	2021-06-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2031313-5
ISSN	1471-0080 ; 1471-0072
ISSN (online)	1471-0080
ISSN	1471-0072
DOI	10.1038/s41580-021-00375-5
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Zs.A 5446: 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)
Zs.MG 26: Show issues

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Article: Actin in membrane trafficking.

Lanzetti, Letizia

Current opinion in cell biology

2007 Volume 19, Issue 4, Page(s) 453–458

Abstract: Actin cytoskeleton remodeling provides the forces required for a variety of cellular processes based on membrane dynamics, such as endocytosis, exocytosis, and vesicular trafficking at the Golgi. All these events are coordinated by networks of associated ...

Abstract	Actin cytoskeleton remodeling provides the forces required for a variety of cellular processes based on membrane dynamics, such as endocytosis, exocytosis, and vesicular trafficking at the Golgi. All these events are coordinated by networks of associated proteins, and some of them are functionally connected with cell migration. The site and the duration of actin polymerization, in connection with vesicle budding and fusion, are tightly controlled by both small GTPases and the large GTPase dynamin. Recent advances in the understanding of the mechanisms coupling actin dynamics with membrane trafficking at the cell surface have been brought by the combined studies of actin polymerizing factors and of the endocytic/exocytic machinery.
MeSH term(s)	Actins/physiology ; Animals ; Cell Membrane/physiology ; Endocytosis/physiology ; Exocytosis/physiology ; Humans ; Models, Biological ; Protein Transport ; rab GTP-Binding Proteins/physiology
Chemical Substances	Actins ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2007-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1026381-0
ISSN	1879-0410 ; 0955-0674
ISSN (online)	1879-0410
ISSN	0955-0674
DOI	10.1016/j.ceb.2007.04.017
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Zs.A 2963: Show issues

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Article: KRAS-Driven Metabolic Rewiring Reveals Novel Actionable Targets in Cancer.

Pupo, Emanuela / Avanzato, Daniele / Middonti, Emanuele / Bussolino, Federico / Lanzetti, Letizia

Frontiers in oncology

2019 Volume 9, Page(s) 848

Abstract: Tumors driven by mutant KRAS are among the most aggressive and refractory to treatment. Unfortunately, despite the efforts, targeting alterations of this GTPase, either directly or by acting on the downstream signaling cascades, has been, so far, largely ...

Abstract	Tumors driven by mutant KRAS are among the most aggressive and refractory to treatment. Unfortunately, despite the efforts, targeting alterations of this GTPase, either directly or by acting on the downstream signaling cascades, has been, so far, largely unsuccessful. However, recently, novel therapeutic opportunities are emerging based on the effect that this oncogenic lesion exerts in rewiring the cancer cell metabolism. Cancer cells that become dependent on KRAS-driven metabolic adaptations are sensitive to the inhibition of these metabolic routes, revealing novel therapeutic windows of intervention. In general, mutant KRAS fosters tumor growth by shifting cancer cell metabolism toward anabolic pathways. Depending on the tumor, KRAS-driven metabolic rewiring occurs by up-regulating rate-limiting enzymes involved in amino acid, fatty acid, or nucleotide biosynthesis, and by stimulating scavenging pathways such as macropinocytosis and autophagy, which, in turn, provide building blocks to the anabolic routes, also maintaining the energy levels and the cell redox potential (1). This review will discuss the most recent findings on mutant KRAS metabolic reliance in tumor models of pancreatic and non-small-cell lung cancer, also highlighting the role that these metabolic adaptations play in resistance to target therapy. The effects of constitutive KRAS activation in glycolysis elevation, amino acids metabolism reprogramming, fatty acid turnover, and nucleotide biosynthesis will be discussed also in the context of different genetic landscapes.
Language	English
Publishing date	2019-08-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2019.00848
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Article ; Online: Emerging functions of the EGFR in cancer.

Sigismund, Sara / Avanzato, Daniele / Lanzetti, Letizia

Molecular oncology

2017 Volume 12, Issue 1, Page(s) 3–20

Abstract: The physiological function of the epidermal growth factor receptor (EGFR) is to regulate epithelial tissue development and homeostasis. In pathological settings, mostly in lung and breast cancer and in glioblastoma, the EGFR is a driver of tumorigenesis. ...

Abstract	The physiological function of the epidermal growth factor receptor (EGFR) is to regulate epithelial tissue development and homeostasis. In pathological settings, mostly in lung and breast cancer and in glioblastoma, the EGFR is a driver of tumorigenesis. Inappropriate activation of the EGFR in cancer mainly results from amplification and point mutations at the genomic locus, but transcriptional upregulation or ligand overproduction due to autocrine/paracrine mechanisms has also been described. Moreover, the EGFR is increasingly recognized as a biomarker of resistance in tumors, as its amplification or secondary mutations have been found to arise under drug pressure. This evidence, in addition to the prominent function that this receptor plays in normal epithelia, has prompted intense investigations into the role of the EGFR both at physiological and at pathological level. Despite the large body of knowledge obtained over the last two decades, previously unrecognized (herein defined as 'noncanonical') functions of the EGFR are currently emerging. Here, we will initially review the canonical ligand-induced EGFR signaling pathway, with particular emphasis to its regulation by endocytosis and subversion in human tumors. We will then focus on the most recent advances in uncovering noncanonical EGFR functions in stress-induced trafficking, autophagy, and energy metabolism, with a perspective on future therapeutic applications.
MeSH term(s)	Animals ; Autophagy/physiology ; Cell Membrane/metabolism ; Endocytosis/physiology ; Endosomes/metabolism ; ErbB Receptors/genetics ; ErbB Receptors/physiology ; Humans ; Ligands ; Mice ; Mice, Knockout ; Neoplasms/pathology ; Stress, Physiological
Chemical Substances	Ligands ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2017-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.12155
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Zs.A 6637: Show issues

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Article ; Online: Behind the Scenes: Endo/Exocytosis in the Acquisition of Metastatic Traits.

Lanzetti, Letizia / Di Fiore, Pier Paolo

Cancer research

2017 Volume 77, Issue 8, Page(s) 1813–1817

Abstract: Alterations of endo/exocytic proteins have long been associated with malignant transformation, and genes encoding membrane trafficking proteins have been identified ... ...

Abstract	Alterations of endo/exocytic proteins have long been associated with malignant transformation, and genes encoding membrane trafficking proteins have been identified as
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Cell Membrane/metabolism ; Endocytosis/physiology ; Exocytosis/physiology ; Humans ; Neoplasm Metastasis ; Neoplasms/metabolism ; Neoplasms/pathology ; rab GTP-Binding Proteins/metabolism
Chemical Substances	rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2017-04-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-16-3403
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Article ; Online: Sema4C/PlexinB2 signaling controls breast cancer cell growth, hormonal dependence and tumorigenic potential.

Gurrapu, Sreeharsha / Pupo, Emanuela / Franzolin, Giulia / Lanzetti, Letizia / Tamagnone, Luca

Cell death and differentiation

2018 Volume 25, Issue 7, Page(s) 1259–1275

Abstract: Semaphorin 4C (Sema4C) expression in human breast cancers correlates with poor disease outcome. Surprisingly, upon knock-down of Sema4C or its receptor PlexinB2 in diverse mammary carcinoma cells (but not their normal counterparts), we observed dramatic ... ...

Abstract	Semaphorin 4C (Sema4C) expression in human breast cancers correlates with poor disease outcome. Surprisingly, upon knock-down of Sema4C or its receptor PlexinB2 in diverse mammary carcinoma cells (but not their normal counterparts), we observed dramatic growth inhibition associated with impairment of G2/M phase transition, cytokinesis defects and the onset of cell senescence. Mechanistically, we demonstrated a Sema4C/PlexinB2/LARG-dependent signaling cascade that is required to maintain critical RhoA-GTP levels in cancer cells. Interestingly, we also found that Sema4C upregulation in luminal-type breast cancer cells drives a dramatic phenotypic change, with disassembly of polarity complexes, mitotic spindle misorientation, cell-cell dissociation and increased migration and invasiveness. We found that this signaling cascade is dependent on the PlexinB2 effectors ErbB2 and RhoA-dependent kinases. Moreover, Sema4C-overexpressing luminal breast cancer cells upregulated the transcription factors Snail, Slug and SOX-2, and formed estrogen-independent metastatic tumors in mice. In sum, our data indicate that Sema4C/PlexinB2 signaling is essential for the growth of breast carcinoma cells, featuring a novel potential therapeutic target. In addition, elevated Sema4C expression enables indolent luminal-type tumors to become resistant to estrogen deprivation, invasive and metastatic in vivo, which could account for its association with a subset of human breast cancers with poor prognosis.
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Estrogens/metabolism ; Estrogens/pharmacology ; Female ; Humans ; MCF-7 Cells ; Mice ; Mice, Nude ; Mice, SCID ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/metabolism ; Semaphorins/genetics ; Semaphorins/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics
Chemical Substances	Estrogens ; Nerve Tissue Proteins ; PLXNB2 protein, human ; Sema4c protein, human ; Semaphorins ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2018-03-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-018-0097-4
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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)
Zs.MG 80: Show issues

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Article ; Online: Kinesin-2 Controls the Motility of RAB5 Endosomes and Their Association with the Spindle in Mitosis.

Pupo, Emanuela / Avanzato, Daniele / Scianna, Marco / Oldani, Amanda / Serini, Guido / Lanzetti, Letizia

International journal of molecular sciences

2018 Volume 19, Issue 9

Abstract: RAB5 is a small GTPase that belongs to the wide family of Rab proteins and localizes on early endosomes. In its active GTP-bound form, RAB5 recruits downstream effectors that, in turn, are responsible for distinct aspects of early endosome function, ... ...

Abstract	RAB5 is a small GTPase that belongs to the wide family of Rab proteins and localizes on early endosomes. In its active GTP-bound form, RAB5 recruits downstream effectors that, in turn, are responsible for distinct aspects of early endosome function, including their movement along microtubules. We previously reported that, at the onset of mitosis, RAB5positive vesicles cluster around the spindle poles and, during metaphase, move along spindle microtubules. RNAi-mediated depletion of the three RAB5 isoforms delays nuclear envelope breakdown at prophase and severely affects chromosome alignment and segregation. Here we show that depletion of the Kinesin-2 motor complex impairs long-range movement of RAB5 endosomes in interphase cells and prevents localization of these vesicles at the spindle during metaphase. Similarly to the effect caused by RAB5 depletion, functional ablation of Kinesin-2 delays nuclear envelope breakdown resulting in prolonged prophase. Altogether these findings suggest that endosomal transport at the onset of mitosis is required to control timing of nuclear envelope breakdown.
MeSH term(s)	Cell Line ; Endosomes/physiology ; Humans ; Interphase ; Kinesin/genetics ; Kinesin/metabolism ; Metaphase ; Microtubules/metabolism ; RNA Interference ; Spindle Apparatus/metabolism ; rab5 GTP-Binding Proteins/metabolism
Chemical Substances	KIF2A protein, human ; RAB5C protein, human (EC 3.6.1.-) ; Kinesin (EC 3.6.4.4) ; rab5 GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2018-08-30
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/ijms19092575
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Article ; Online: Rebound Effects Caused by Withdrawal of MET Kinase Inhibitor Are Quenched by a MET Therapeutic Antibody.

Pupo, Emanuela / Ducano, Nadia / Lupo, Barbara / Vigna, Elisa / Avanzato, Daniele / Perera, Timothy / Trusolino, Livio / Lanzetti, Letizia / Comoglio, Paolo M

Cancer research

2016 Volume 76, Issue 17, Page(s) 5019–5029

Abstract: MET oncogene amplification is emerging as a major mechanism of acquired resistance to EGFR-directed therapy in lung and colorectal cancers. Furthermore, MET amplification predicts responsiveness to MET inhibitors currently in clinical trials. Among the ... ...

Abstract	MET oncogene amplification is emerging as a major mechanism of acquired resistance to EGFR-directed therapy in lung and colorectal cancers. Furthermore, MET amplification predicts responsiveness to MET inhibitors currently in clinical trials. Among the anti-MET drugs available, ATP-competitive small-molecule kinase inhibitors abrogate receptor autophosphorylation and downstream activation of ERK1/2 and AKT, resulting in cell-cycle arrest. However, this antiproliferative effect allows persistence of a pool of cancer cells that are quiescent but alive. Once the inhibition is removed, rebound activation of MET-driven cell proliferative pathways and tumor growth may occur, an adverse event observed frequently in clinical settings after drug discontinuation. Here we show that inhibitor withdrawal prompts receptor phosphorylation to levels higher than those displayed at steady-state and generates a rebound effect pushing quiescent cancer cells back into the cell cycle, both in vitro and in experimental tumor models in vivo Mechanistically, we found that inhibitor treatment blocks MET endocytosis, causing a local increase in the number of receptors at the plasma membrane. Upon inhibitor washout, the receptor is readily rephosphorylated. The initial phosphorylation is not only increased but also prolonged in duration due to downmodulation of a phosphatase-mediated MET-negative feedback loop, which accompanies receptor internalization. Notably, treatment with a MET therapeutic antibody that induces proteolytic cleavage of the receptor at the cell surface substantially prevents this rebound effect, providing a rationale to combine or alternate these mechanistically different types of MET-targeted therapy. Cancer Res; 76(17); 5019-29. ©2016 AACR.
MeSH term(s)	Animals ; Antibodies/pharmacology ; Antineoplastic Agents/pharmacology ; Blotting, Western ; Cell Line, Tumor ; Drug Resistance, Neoplasm/drug effects ; Female ; Fluorescent Antibody Technique ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Microscopy, Confocal ; Neoplasm Recurrence, Local/metabolism ; Neoplasm Recurrence, Local/pathology ; Neoplasms, Experimental/metabolism ; Neoplasms, Experimental/pathology ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-met/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies ; Antineoplastic Agents ; Protein Kinase Inhibitors ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
Language	English
Publishing date	2016-09-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-15-3107
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