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Book ; Online ; E-Book: TCTP/tpt1 - remodeling signaling from stem cell to disease

Telerman, Adam / Amson, Robert

(Results and problems in cell differentiation ; 64)

2017

Author's details	Adam Telerman, Robert Amson editors
Series title	Results and problems in cell differentiation ; 64
Collection
Keywords	Translationally Controlled Tumor Protein ; histamine-releasing factor ; tumor reversion ; cell fate ; cell signalling
Subject code	610
Language	English
Size	1 Online-Ressource (x, 309 Seiten), Illustrationen, Diagramme
Publisher	Springer
Publishing place	Cham
Publishing country	Switzerland
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019516875
ISBN	978-3-319-67591-6 ; 9783319675909 ; 3-319-67591-5 ; 3319675907
DOI	10.1007/978-3-319-67591-6
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article: Introduction: How We Encountered TCTP and Our Purpose in Studying It.

Telerman, Adam / Amson, Robert

Results and problems in cell differentiation

2018 Volume 64, Page(s) 1–8

Abstract: In this brief introduction, we describe our encounter with TCTP. Back in 2000, we discovered TCTP in two quite different ways: first, we looked at protein partners of TSAP6 and one of them was TCTP. Then, in collaboration with Sidney Brenner, we ... ...

Abstract	In this brief introduction, we describe our encounter with TCTP. Back in 2000, we discovered TCTP in two quite different ways: first, we looked at protein partners of TSAP6 and one of them was TCTP. Then, in collaboration with Sidney Brenner, we performed a high-throughput differential screening comparing the parental cancer cells with revertants. The results indicated that TCTP was of the most differentially expressed genes. These two approaches were carried out only months apart. They guided our research and led to the discoveries of drugs that inhibit the function of TCTP. Much of the preclinical data on sertraline as an inhibitor of TCTP in cancer were obtained with Judith Karp at Johns Hopkins. This drug is now given in combination with Ara-C to patients in a phase I clinical trial for Acute Myeloid Leukemia. We will here detail how all this happened in our lab while working around one central project: tumor reversion.
MeSH term(s)	Biomarkers, Tumor/antagonists & inhibitors ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/history ; Biomarkers, Tumor/metabolism ; Cell Cycle Proteins ; Clinical Trials, Phase I as Topic ; Cytarabine/administration & dosage ; Cytarabine/therapeutic use ; Gene Expression Regulation, Neoplastic ; History, 21st Century ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Oncogene Proteins/antagonists & inhibitors ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; Oxidoreductases ; Sertraline/administration & dosage ; Sertraline/pharmacology ; Sertraline/therapeutic use
Chemical Substances	Biomarkers, Tumor ; Cell Cycle Proteins ; Oncogene Proteins ; tumor protein, translationally-controlled 1 ; Cytarabine (04079A1RDZ) ; Oxidoreductases (EC 1.-) ; STEAP3 protein, human (EC 1.-) ; Sertraline (QUC7NX6WMB)
Language	English
Publishing date	2018-01-04
Publishing country	Germany
Document type	Historical Article ; Journal Article
ISSN	0080-1844
ISSN	0080-1844
DOI	10.1007/978-3-319-67591-6_1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Topoisomerase II is regulated by translationally controlled tumor protein for cell survival during organ growth in Drosophila.

Yang, Dae-Wook / Mok, Jung-Wan / Telerman, Stephanie B / Amson, Robert / Telerman, Adam / Choi, Kwang-Wook

Cell death & disease

2021 Volume 12, Issue 9, Page(s) 811

Abstract: Regulation of cell survival is critical for organ development. Translationally controlled tumor protein (TCTP) is a conserved protein family implicated in the control of cell survival during normal development and tumorigenesis. Previously, we have ... ...

Abstract	Regulation of cell survival is critical for organ development. Translationally controlled tumor protein (TCTP) is a conserved protein family implicated in the control of cell survival during normal development and tumorigenesis. Previously, we have identified a human Topoisomerase II (TOP2) as a TCTP partner, but its role in vivo has been unknown. To determine the significance of this interaction, we examined their roles in developing Drosophila organs. Top2 RNAi in the wing disc leads to tissue reduction and caspase activation, indicating the essential role of Top2 for cell survival. Top2 RNAi in the eye disc also causes loss of eye and head tissues. Tctp RNAi enhances the phenotypes of Top2 RNAi. The depletion of Tctp reduces Top2 levels in the wing disc and vice versa. Wing size is reduced by Top2 overexpression, implying that proper regulation of Top2 level is important for normal organ development. The wing phenotype of Tctp RNAi is partially suppressed by Top2 overexpression. This study suggests that mutual regulation of Tctp and Top2 protein levels is critical for cell survival during organ development.
MeSH term(s)	Animals ; Cell Survival/genetics ; DNA Topoisomerases, Type II/metabolism ; Drosophila Proteins/metabolism ; Drosophila melanogaster/cytology ; Drosophila melanogaster/genetics ; Drosophila melanogaster/growth & development ; Epistasis, Genetic ; Female ; Green Fluorescent Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Male ; Organogenesis/genetics ; Phenotype ; RNA Interference ; Wings, Animal/growth & development
Chemical Substances	Drosophila Proteins ; Intracellular Signaling Peptides and Proteins ; TCTP protein, Drosophila ; Green Fluorescent Proteins (147336-22-9) ; DNA Topoisomerases, Type II (EC 5.99.1.3) ; Top2 protein, Drosophila (EC 5.99.1.3)
Language	English
Publishing date	2021-08-27
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/s41419-021-04091-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: TCTP regulates genotoxic stress and tumorigenicity via intercellular vesicular signaling.

EMBO reports

2024 Volume 25, Issue 4, Page(s) 1962–1986

Abstract: Oncogenic intercellular signaling is regulated by extracellular vesicles (EVs), but the underlying mechanisms remain mostly unclear. Since TCTP (translationally controlled tumor protein) is an EV component, we investigated whether it has a role in ... ...

Abstract	Oncogenic intercellular signaling is regulated by extracellular vesicles (EVs), but the underlying mechanisms remain mostly unclear. Since TCTP (translationally controlled tumor protein) is an EV component, we investigated whether it has a role in genotoxic stress signaling and malignant transformation. By generating a Tctp-inducible knockout mouse model (Tctp
MeSH term(s)	Mice ; Humans ; Animals ; Biomarkers, Tumor/metabolism ; Neoplasms/pathology ; Apoptosis ; Signal Transduction
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2024-03-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.1038/s44319-024-00108-7
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Article: Targeting TCTP with Sertraline and Thioridazine in Cancer Treatment.

Amson, Robert / Auclair, Christian / André, Fabrice / Karp, Judith / Telerman, Adam

Results and problems in cell differentiation

2017 Volume 64, Page(s) 283–290

Abstract: We have initially demonstrated in knocking down experiments that decreasing TCTP in cancer cells leads in some tissues to cell death while in others to a complete reorganization of the tumor into architectural structures reminiscent of normal ones. Based ...

Abstract	We have initially demonstrated in knocking down experiments that decreasing TCTP in cancer cells leads in some tissues to cell death while in others to a complete reorganization of the tumor into architectural structures reminiscent of normal ones. Based on these experiments and a series of other findings confirming the key role of TCTP in cancer, it became important to find pharmacological compounds to inhibit its function, and this became for us a priority. In the present text, we explain in detail the experiments that were performed and the perspectives of sertraline in cancer treatment, as this became today a reality with a clinical study that started in collaboration with Columbia University and Johns Hopkins University.
MeSH term(s)	Biomarkers, Tumor/antagonists & inhibitors ; Biomarkers, Tumor/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Sertraline/pharmacology ; Sertraline/therapeutic use ; Thioridazine/pharmacology ; Thioridazine/therapeutic use
Chemical Substances	Biomarkers, Tumor ; tumor protein, translationally-controlled 1 ; Thioridazine (N3D6TG58NI) ; Sertraline (QUC7NX6WMB)
Language	English
Publishing date	2017-11-22
Publishing country	Germany
Document type	Journal Article
ISSN	0080-1844
ISSN	0080-1844
DOI	10.1007/978-3-319-67591-6_15
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Lessons from tumor reversion for cancer treatment.

Amson, Robert / Karp, Judith E / Telerman, Adam

Current opinion in oncology

2013 Volume 25, Issue 1, Page(s) 59–65

Abstract: Purpose of review: Tumor reversion is the biological process by which highly tumorigenic cells lose at great extent or entirely their malignant phenotype. The purpose of our research is to understand the molecular program of tumor reversion and its ... ...

Abstract	Purpose of review: Tumor reversion is the biological process by which highly tumorigenic cells lose at great extent or entirely their malignant phenotype. The purpose of our research is to understand the molecular program of tumor reversion and its clinical application. We first established biological models of reversion, which was done by deriving revertant cells from different tumors. Secondly, the molecular program that could override the malignant phenotype was assessed. Differential gene-expression profiling showed that at least 300 genes are implicated in this reversion process such as SIAH-1, PS1, TSAP6, and, most importantly, translationally controlled tumor protein (TPT1/TCTP). Decreasing TPT1/TCTP is key in reprogramming malignant cells, including cancer stem cells. Recent findings: Recent findings indicate that TPT1/TCTP regulates the P53-MDM2-Numb axis. Notably, TPT1/TCTP and p53 are implicated in a reciprocal negative-feedback loop. TPT1/TCTP is a highly significant prognostic factor in breast cancer. Sertraline and thioridazine interfere with this repressive feedback by targeting directly TPT1/TCTP and inhibiting its binding to MDM2, restoring wildtype p53 function. Combining sertraline with classical drugs such as Ara-C in acute myeloid leukemia may be also beneficial. Summary: In this review, we discuss some of these reversion pathways and how this approach could open a new route to cancer treatment.
MeSH term(s)	Antidepressive Agents/therapeutic use ; Antineoplastic Agents/therapeutic use ; Antipsychotic Agents/therapeutic use ; Biomarkers, Tumor/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Nuclear Proteins/genetics ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Antidepressive Agents ; Antineoplastic Agents ; Antipsychotic Agents ; Biomarkers, Tumor ; Nuclear Proteins ; Tumor Suppressor Protein p53 ; tumor protein, translationally-controlled 1
Language	English
Publishing date	2013-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1049384-0
ISSN	1531-703X ; 1040-8746
ISSN (online)	1531-703X
ISSN	1040-8746
DOI	10.1097/CCO.0b013e32835b7d21
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Article ; Online: The molecular programme of tumour reversion: the steps beyond malignant transformation.

Telerman, Adam / Amson, Robert

Nature reviews. Cancer

2009 Volume 9, Issue 3, Page(s) 206–216

Abstract: How cells become malignant has preoccupied scientists for over a century. However, the converse question is also valid: are tumour cells capable of reverting from their malignant state? Askanazy's studies in 1907 indicated that teratoma cells could ... ...

Abstract	How cells become malignant has preoccupied scientists for over a century. However, the converse question is also valid: are tumour cells capable of reverting from their malignant state? Askanazy's studies in 1907 indicated that teratoma cells could differentiate into normal somatic tissues and current evidence indicates that some tumour cells have acquired the molecular circuitry that results in the negation of chromosomal instability, translocations, oncogene activation and loss of tumour suppressor genes. Studying these extremely rare events of tumour reversion and deciphering these pathways, which involve SIAH1, presenilin 1, TSAP6 and translationally controlled tumour protein (TCTP), could lead to new avenues in cancer treatment.
MeSH term(s)	Animals ; Biomarkers, Tumor/physiology ; Cell Cycle Proteins ; Cell Transformation, Neoplastic ; Humans ; Models, Biological ; Neoplasms/drug therapy ; Neoplasms/genetics ; Nuclear Proteins/physiology ; Oncogene Proteins/physiology ; Oxidoreductases ; Presenilin-1/physiology ; Ubiquitin-Protein Ligases/physiology
Chemical Substances	Biomarkers, Tumor ; Cell Cycle Proteins ; Nuclear Proteins ; Oncogene Proteins ; Presenilin-1 ; tumor protein, translationally-controlled 1 ; Oxidoreductases (EC 1.-) ; STEAP3 protein, human (EC 1.-) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; seven in absentia proteins (EC 2.3.2.27)
Language	English
Publishing date	2009-01-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/nrc2589
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Article ; Online: Tumor reversion holds promise.

Telerman, Adam / Amson, Robert / Hendrix, Mary J C

Oncotarget

2011 Volume 1, Issue 4, Page(s) 233–234

MeSH term(s)	Antineoplastic Agents/therapeutic use ; Drug Screening Assays, Antitumor ; GPI-Linked Proteins/genetics ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Phenotype ; Promoter Regions, Genetic
Chemical Substances	Antineoplastic Agents ; GPI-Linked Proteins ; RECK protein, human
Language	English
Publishing date	2011-02-08
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.100803
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Acetylation of translationally controlled tumor protein promotes its degradation through chaperone-mediated autophagy.

Bonhoure, Anne / Vallentin, Alice / Martin, Marianne / Senff-Ribeiro, Andrea / Amson, Robert / Telerman, Adam / Vidal, Michel

European journal of cell biology

2017 Volume 96, Issue 2, Page(s) 83–98

Abstract: Translationally controlled tumor protein (Tpt1/TCTP) is a multi-functional cytosolic protein whose cellular levels are finely tuned. TCTP regulates protein behavior by favoring stabilization of protein partners or on the contrary by promoting degradation ...

Abstract	Translationally controlled tumor protein (Tpt1/TCTP) is a multi-functional cytosolic protein whose cellular levels are finely tuned. TCTP regulates protein behavior by favoring stabilization of protein partners or on the contrary by promoting degradation of others. TCTP has been shown to be transcriptionally and translationally regulated, but much less is known about its degradation process. In this study, we present evidence that chaperone-mediated autophagy (CMA) contributes to TCTP regulation. CMA allows lysosomal degradation of specific cytosolic proteins on a molecule-by-molecule basis. It contributes to cellular homeostasis especially by acting as a quality control for cytosolic proteins in response to stress and as a way of regulating the level of specific proteins. Using a variety of approaches, we show that CMA degradation of TCTP is Hsc70 and LAMP-2A dependent. Our data indicate that (i) TCTP directly interacts with Hsc70; (ii) silencing LAMP-2A in MEFs using siRNA leads to inhibition of TCTP downregulation; (iii) TCTP is relocalized from a diffuse cytosolic pattern to a punctate lysosomal pattern when CMA is upregulated; (iv) TCTP is degraded in vitro by purified lysosomes. Importantly, using lysine-mutated forms of TCTP, we show that acetylation of Lysine 19 generates a KFERQ-like motif and promotes binding to Hsc70, lysosome targeting and TCTP degradation by CMA. Altogether these results indicate that TCTP is degraded by chaperone-mediated autophagy in an acetylation dependent manner.
MeSH term(s)	Acetylation ; Animals ; Autophagy/physiology ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/metabolism ; Down-Regulation ; Fibroblasts/metabolism ; HSP70 Heat-Shock Proteins/metabolism ; HeLa Cells ; Humans ; Lysosomes/metabolism ; MCF-7 Cells ; Metabolic Networks and Pathways ; Mice ; Molecular Chaperones/metabolism ; Neoplasm Proteins/metabolism ; Protein Processing, Post-Translational ; Proteolysis
Chemical Substances	Biomarkers, Tumor ; HSP70 Heat-Shock Proteins ; Molecular Chaperones ; Neoplasm Proteins ; tumor protein, translationally-controlled 1
Language	English
Publishing date	2017-03
Publishing country	Germany
Document type	Journal Article
ZDB-ID	391967-5
ISSN	1618-1298 ; 0070-2463 ; 0171-9335
ISSN (online)	1618-1298
ISSN	0070-2463 ; 0171-9335
DOI	10.1016/j.ejcb.2016.12.002
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Article ; Online: Obituary: Jean Dausset.

Telerman, Adam / Amson, Robert / Demant, Peter / Marrack, Philippa

Immunity

2009 Volume 31, Issue 2, Page(s) 171–173

MeSH term(s)	France ; Genetic Predisposition to Disease/history ; Genetics, Medical/history ; History, 20th Century ; History, 21st Century ; Humans ; Major Histocompatibility Complex/genetics ; Nobel Prize
Language	English
Publishing date	2009-07-01
Publishing country	United States
Document type	Biography ; Historical Article ; Journal Article ; Portrait
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2009.07.004
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