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Article ; Online: Crosstalk between TGF-β and EGF receptors via direct phosphorylation.

Moustakas, Aristidis

2024 Volume 223, Issue 4

Abstract: Aristidis Moustakas discusses work from Ye-Guang Chen and colleagues (https://doi.org/10.1083/jcb ...

Abstract	Aristidis Moustakas discusses work from Ye-Guang Chen and colleagues (https://doi.org/10.1083/jcb.202307138) on a new mechanism by which TGF-β modulates HER2 signaling in mammary epithelia.
MeSH term(s)	ErbB Receptors/genetics ; Phosphorylation ; Transforming Growth Factor beta ; Animals
Chemical Substances	ErbB Receptors (EC 2.7.10.1) ; Transforming Growth Factor beta
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.202403075
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Article ; Online: Unboxing the network among long non-coding RNAs and TGF-β signaling in cancer.

Rodrigues-Junior, Dorival Mendes / Moustakas, Aristidis

Upsala journal of medical sciences

2024 Volume 129

Abstract: Deeper analysis of molecular mechanisms arising in tumor cells is an unmet need to provide new diagnostic and therapeutic strategies to prevent and treat tumors. The transforming growth factor β (TGF-β) signaling has been steadily featured in tumor ... ...

Abstract	Deeper analysis of molecular mechanisms arising in tumor cells is an unmet need to provide new diagnostic and therapeutic strategies to prevent and treat tumors. The transforming growth factor β (TGF-β) signaling has been steadily featured in tumor biology and linked to poor prognosis of cancer patients. One pro-tumorigenic mechanism induced by TGF-β is the epithelial-to-mesenchymal transition (EMT), which can initiate cancer dissemination, enrich the tumor stem cell population, and increase chemoresistance. TGF-β signals via SMAD proteins, ubiquitin ligases, and protein kinases and modulates the expression of protein-coding and non-coding RNA genes, including those encoding larger than 500 nt transcripts, defined as long non-coding RNAs (lncRNAs). Several reports have shown lncRNAs regulating malignant phenotypes by directly affecting epigenetic processes, transcription, and post-transcriptional regulation. Thus, this review aims to update and summarize the impact of TGF-β signaling on the expression of lncRNAs and the function of such lncRNAs as regulators of TGF-β signaling, and how these networks might impact specific hallmarks of cancer.
MeSH term(s)	Humans ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Neoplasms/genetics ; Signal Transduction ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic
Chemical Substances	Transforming Growth Factor beta ; RNA, Long Noncoding
Language	English
Publishing date	2024-03-26
Publishing country	Sweden
Document type	Journal Article ; Review
ZDB-ID	183949-4
ISSN	2000-1967 ; 0300-9734
ISSN (online)	2000-1967
ISSN	0300-9734
DOI	10.48101/ujms.v129.10614
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Article ; Online: Cellular heterogeneity in pancreatic cancer: the different faces of gremlin action.

Moustakas, Aristidis / Löhr, J Matthias / Heuchel, Rainer L

Signal transduction and targeted therapy

2022 Volume 7, Issue 1, Page(s) 364

MeSH term(s)	Humans ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms
Language	English
Publishing date	2022-10-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2886872-9
ISSN	2059-3635 ; 2095-9907
ISSN (online)	2059-3635
ISSN	2095-9907
DOI	10.1038/s41392-022-01203-8
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Article ; Online: The mitotic checkpoint protein kinase BUB1 is an engine in the TGF-β signaling apparatus.

Moustakas, Aristidis

Science signaling

2015 Volume 8, Issue 359, Page(s) fs1

Abstract: The transforming growth factor-β (TGF-β) pathway mediates critical events in cell behavior that contribute to development and disease. The mitotic checkpoint guarantees faithful chromosomal segregation during cell division. In the 6 January 2015 issue of ...

Abstract	The transforming growth factor-β (TGF-β) pathway mediates critical events in cell behavior that contribute to development and disease. The mitotic checkpoint guarantees faithful chromosomal segregation during cell division. In the 6 January 2015 issue of Science Signaling, Nyati et al. reported that the mitotic checkpoint kinase BUB1 promotes the activity of TGF-β receptors, which adds new molecular links between these fundamental biological processes.
MeSH term(s)	Animals ; Humans ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction/physiology ; Smad Proteins, Receptor-Regulated/metabolism ; Transforming Growth Factor beta/physiology
Chemical Substances	Receptors, Transforming Growth Factor beta ; Smad Proteins, Receptor-Regulated ; Transforming Growth Factor beta ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2015-01-13
Publishing country	United States
Document type	Comment ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.aaa4636
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Article ; Online: TGF-β Signaling.

Tzavlaki, Kalliopi / Moustakas, Aristidis

Biomolecules

2020 Volume 10, Issue 3

Abstract: Transforming growth factor-β (TGF-β) represents an evolutionarily conserved family of secreted polypeptide factors that regulate many aspects of physiological embryogenesis and adult tissue homeostasis. The TGF-β family members are also involved in ... ...

Abstract	Transforming growth factor-β (TGF-β) represents an evolutionarily conserved family of secreted polypeptide factors that regulate many aspects of physiological embryogenesis and adult tissue homeostasis. The TGF-β family members are also involved in pathophysiological mechanisms that underlie many diseases. Although the family comprises many factors, which exhibit cell type-specific and developmental stage-dependent biological actions, they all signal via conserved signaling pathways. The signaling mechanisms of the TGF-β family are controlled at the extracellular level, where ligand secretion, deposition to the extracellular matrix and activation prior to signaling play important roles. At the plasma membrane level, TGF-βs associate with receptor kinases that mediate phosphorylation-dependent signaling to downstream mediators, mainly the SMAD proteins, and mediate oligomerization-dependent signaling to ubiquitin ligases and intracellular protein kinases. The interplay between SMADs and other signaling proteins mediate regulatory signals that control expression of target genes, RNA processing at multiple levels, mRNA translation and nuclear or cytoplasmic protein regulation. This article emphasizes signaling mechanisms and the importance of biochemical control in executing biological functions by the prototype member of the family, TGF-β.
MeSH term(s)	Animals ; Cell Membrane/metabolism ; Extracellular Matrix/metabolism ; Humans ; Protein Kinases/metabolism ; RNA Processing, Post-Transcriptional ; Signal Transduction ; Smad Proteins/metabolism ; Transforming Growth Factor beta/metabolism ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Smad Proteins ; Transforming Growth Factor beta ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2020-03-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10030487
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Article ; Online: Long non-coding RNAs and TGF-β signaling in cancer.

Papoutsoglou, Panagiotis / Moustakas, Aristidis

Cancer science

2020 Volume 111, Issue 8, Page(s) 2672–2681

Abstract: Cancer is driven by genetic mutations in oncogenes and tumor suppressor genes and by cellular events that develop a misregulated molecular microenvironment in the growing tumor tissue. The tumor microenvironment is guided by the excessive action of ... ...

Abstract	Cancer is driven by genetic mutations in oncogenes and tumor suppressor genes and by cellular events that develop a misregulated molecular microenvironment in the growing tumor tissue. The tumor microenvironment is guided by the excessive action of specific cytokines including transforming growth factor-β (TGF-β), which normally controls embryonic development and the homeostasis of young or adult tissues. As a consequence of the genetic alterations generating a given tumor, TGF-β can preserve its homeostatic function and attempt to limit neoplastic expansion, whereas, once the tumor has progressed to an aggressive stage, TGF-β can synergize with various oncogenic stimuli to facilitate tumor invasiveness and metastasis. TGF-β signaling mechanisms via Smad proteins, various ubiquitin ligases, and protein kinases are relatively well understood. Such mechanisms regulate the expression of genes encoding proteins or non-coding RNAs. Among non-coding RNAs, much has been understood regarding the regulation and function of microRNAs, whereas the role of long non-coding RNAs is still emerging. This article emphasizes TGF-β signaling mechanisms leading to the regulation of non-coding genes, the function of such non-coding RNAs as regulators of TGF-β signaling, and the contribution of these mechanisms in specific hallmarks of cancer.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Cell Line, Tumor ; Feedback, Physiological ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasm Invasiveness/genetics ; Neoplasms/genetics ; Neoplasms/pathology ; RNA, Long Noncoding/metabolism ; Signal Transduction/genetics ; Smad Proteins/metabolism ; Transforming Growth Factor beta/metabolism ; Tumor Microenvironment/genetics
Chemical Substances	RNA, Long Noncoding ; Smad Proteins ; Transforming Growth Factor beta
Language	English
Publishing date	2020-06-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1347-9032
ISSN (online)	1349-7006
ISSN	1347-9032
DOI	10.1111/cas.14509
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Article: Extracellular Vesicles and Transforming Growth Factor β Signaling in Cancer.

Rodrigues-Junior, Dorival Mendes / Tsirigoti, Chrysoula / Lim, Sai Kiang / Heldin, Carl-Henrik / Moustakas, Aristidis

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 849938

Abstract: Complexity in mechanisms that drive cancer development and progression is exemplified by the transforming growth factor β (TGF-β) signaling pathway, which suppresses early-stage hyperplasia, yet assists aggressive tumors to achieve metastasis. Of note, ... ...

Abstract	Complexity in mechanisms that drive cancer development and progression is exemplified by the transforming growth factor β (TGF-β) signaling pathway, which suppresses early-stage hyperplasia, yet assists aggressive tumors to achieve metastasis. Of note, several molecules, including mRNAs, non-coding RNAs, and proteins known to be associated with the TGF-β pathway have been reported as constituents in the cargo of extracellular vesicles (EVs). EVs are secreted vesicles delimited by a lipid bilayer and play critical functions in intercellular communication, including regulation of the tumor microenvironment and cancer development. Thus, this review aims at summarizing the impact of EVs on TGF-β signaling by focusing on mechanisms by which EV cargo can influence tumorigenesis, metastatic spread, immune evasion and response to anti-cancer treatment. Moreover, we emphasize the potential of TGF-β-related molecules present in circulating EVs as useful biomarkers of prognosis, diagnosis, and prediction of response to treatment in cancer patients.
Language	English
Publishing date	2022-04-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.849938
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Article ; Online: Epithelial-Mesenchymal Transition and Metastasis under the Control of Transforming Growth Factor β.

Tsubakihara, Yutaro / Moustakas, Aristidis

International journal of molecular sciences

2018 Volume 19, Issue 11

Abstract: Metastasis of tumor cells from primary sites of malignancy to neighboring stromal tissue or distant localities entails in several instances, but not in every case, the epithelial-mesenchymal transition (EMT). EMT weakens the strong adhesion forces ... ...

Abstract	Metastasis of tumor cells from primary sites of malignancy to neighboring stromal tissue or distant localities entails in several instances, but not in every case, the epithelial-mesenchymal transition (EMT). EMT weakens the strong adhesion forces between differentiated epithelial cells so that carcinoma cells can achieve solitary or collective motility, which makes the EMT an intuitive mechanism for the initiation of tumor metastasis. EMT initiates after primary oncogenic events lead to secondary secretion of cytokines. The interaction between tumor-secreted cytokines and oncogenic stimuli facilitates EMT progression. A classic case of this mechanism is the cooperation between oncogenic Ras and the transforming growth factor β (TGFβ). The power of TGFβ to mediate EMT during metastasis depends on versatile signaling crosstalk and on the regulation of successive waves of expression of many other cytokines and the progressive remodeling of the extracellular matrix that facilitates motility through basement membranes. Since metastasis involves many organs in the body, whereas EMT affects carcinoma cell differentiation locally, it has frequently been debated whether EMT truly contributes to metastasis. Despite controversies, studies of circulating tumor cells, studies of acquired chemoresistance by metastatic cells, and several (but not all) metastatic animal models, support a link between EMT and metastasis, with TGFβ, often being a common denominator in this link. This article aims at discussing mechanistic cases where TGFβ signaling and EMT facilitate tumor cell dissemination.
MeSH term(s)	Animals ; Epithelial-Mesenchymal Transition/genetics ; Humans ; Models, Biological ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/pathology ; Signal Transduction ; Transcription Factors/metabolism ; Transforming Growth Factor beta/metabolism
Chemical Substances	Transcription Factors ; Transforming Growth Factor beta
Language	English
Publishing date	2018-11-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19113672
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Article ; Online: Endothelial-Tumor Cell Interaction in Brain and CNS Malignancies.

Peleli, Maria / Moustakas, Aristidis / Papapetropoulos, Andreas

International journal of molecular sciences

2020 Volume 21, Issue 19

Abstract: Glioblastoma and other brain or CNS malignancies (like neuroblastoma and medulloblastoma) are difficult to treat and are characterized by excessive vascularization that favors further tumor growth. Since the mean overall survival of these types of ... ...

Abstract	Glioblastoma and other brain or CNS malignancies (like neuroblastoma and medulloblastoma) are difficult to treat and are characterized by excessive vascularization that favors further tumor growth. Since the mean overall survival of these types of diseases is low, the finding of new therapeutic approaches is imperative. In this review, we discuss the importance of the interaction between the endothelium and the tumor cells in brain and CNS malignancies. The different mechanisms of formation of new vessels that supply the tumor with nutrients are discussed. We also describe how the tumor cells (TC) alter the endothelial cell (EC) physiology in a way that favors tumorigenesis. In particular, mechanisms of EC-TC interaction are described such as (a) communication using secreted growth factors (i.e., VEGF, TGF-β), (b) intercellular communication through gap junctions (i.e., Cx43), and (c) indirect interaction via intermediate cell types (pericytes, astrocytes, neurons, and immune cells). At the signaling level, we outline the role of important mediators, like the gasotransmitter nitric oxide and different types of reactive oxygen species and the systems producing them. Finally, we briefly discuss the current antiangiogenic therapies used against brain and CNS tumors and the potential of new pharmacological interventions that target the EC-TC interaction.
MeSH term(s)	Animals ; Brain/blood supply ; Brain Neoplasms/physiopathology ; Cell Communication ; Central Nervous System/blood supply ; Central Nervous System Neoplasms/physiopathology ; Endothelial Cells/physiology ; Gap Junctions/physiology ; Glioblastoma/physiopathology ; Humans ; Neovascularization, Pathologic ; Transforming Growth Factor beta/physiology ; Vascular Endothelial Growth Factor A/physiology
Chemical Substances	Transforming Growth Factor beta ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2020-10-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21197371
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Article ; Online: Loss of SNAI1 induces cellular plasticity in invasive triple-negative breast cancer cells.

Tsirigoti, Chrysoula / Ali, Mohamad Moustafa / Maturi, Varun / Heldin, Carl-Henrik / Moustakas, Aristidis

Cell death & disease

2022 Volume 13, Issue 9, Page(s) 832

Abstract: The transcription factor SNAI1 mediates epithelial-mesenchymal transition, fibroblast activation and controls inter-tissue migration. High SNAI1 expression characterizes metastatic triple-negative breast carcinomas, and its knockout by CRISPR/Cas9 ... ...

Abstract	The transcription factor SNAI1 mediates epithelial-mesenchymal transition, fibroblast activation and controls inter-tissue migration. High SNAI1 expression characterizes metastatic triple-negative breast carcinomas, and its knockout by CRISPR/Cas9 uncovered an epithelio-mesenchymal phenotype accompanied by reduced signaling by the cytokine TGFβ. The SNAI1 knockout cells exhibited plasticity in differentiation, drifting towards the luminal phenotype, gained stemness potential and could differentiate into acinar mammospheres in 3D culture. Loss of SNAI1 de-repressed the transcription factor FOXA1, a pioneering factor of mammary luminal progenitors. FOXA1 induced a specific gene program, including the androgen receptor (AR). Inhibiting AR via a specific antagonist regenerated the basal phenotype and blocked acinar differentiation. Thus, loss of SNAI1 in the context of triple-negative breast carcinoma cells promotes an intermediary luminal progenitor phenotype that gains differentiation plasticity based on the dual transcriptional action of FOXA1 and AR. This function of SNAI1 provides means to separate cell invasiveness from progenitor cell de-differentiation as independent cellular programs.
MeSH term(s)	Breast Neoplasms ; Cell Line, Tumor ; Cell Plasticity/genetics ; Epithelial-Mesenchymal Transition/genetics ; Female ; Humans ; Receptors, Androgen/metabolism ; Snail Family Transcription Factors/genetics ; Transforming Growth Factor beta ; Triple Negative Breast Neoplasms/genetics
Chemical Substances	Receptors, Androgen ; SNAI1 protein, human ; Snail Family Transcription Factors ; Transforming Growth Factor beta
Language	English
Publishing date	2022-09-28
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/s41419-022-05280-z
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