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Article ; Online: TGFß1 Stimulates Lymphatic Endothelial Cells to Produce IL7 and IL15, Which Act as Chemotactic Factors for Breast Cancer Cells with Mesenchymal Properties.

Giotopoulou, Nikolina / Shi, Wenyang / Parniewska, Malgorzata Maria / Sun, Wenwen / Fuxe, Jonas

Journal of mammary gland biology and neoplasia

2023 Volume 28, Issue 1, Page(s) 25

Abstract: The lymphatic system is a major gateway for tumor cell dissemination but the mechanisms of how tumor cells gain access to lymphatic vessels are not completely understood. Breast cancer cells undergoing epithelial-mesenchymal transition (EMT) gain ... ...

Abstract	The lymphatic system is a major gateway for tumor cell dissemination but the mechanisms of how tumor cells gain access to lymphatic vessels are not completely understood. Breast cancer cells undergoing epithelial-mesenchymal transition (EMT) gain invasive and migratory properties. Overexpression of the cytokine transforming growth factor β1 (TGFβ1), a potent inducer of EMT, is frequently detected in the tumor microenvironment and correlates with invasion and lymph metastasis. Recently, we reported that TGFβ1 stimulated breast cancer cells with mesenchymal properties to migrate in a targeted fashion towards the lymphatic system via CCR7/CCL21-mediated chemotaxis, similar to dendritic cells during inflammation. Here, we aimed to identify additional chemotactic factors and corresponding receptors that could be involved in guiding breast cancer cells through the lymphatic system. Through a combination of RNA sequencing analysis, database screening and invasion assays we identified IL7/IL7R and IL15/IL15R as pairs of chemokines and receptors with potential roles in promoting chemotactic migration of breast cancer cells with mesenchymal properties towards the lymphatics. The results demonstrate the capacity of TGFβ1 to orchestrate crosstalk between tumor cells and lymphatic endothelial cells and warrant further studies to explore the roles of IL7 and IL15 in promoting lymph metastasis of breast cancer.
MeSH term(s)	Humans ; Chemotactic Factors ; Endothelial Cells ; Interleukin-15 ; Interleukin-7 ; Lymphatic Metastasis ; Lymphatic Vessels ; Tumor Microenvironment ; Breast Neoplasms ; Epithelial-Mesenchymal Transition
Chemical Substances	Chemotactic Factors ; Interleukin-15 ; Interleukin-7
Language	English
Publishing date	2023-12-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1327345-0
ISSN	1573-7039 ; 1083-3021
ISSN (online)	1573-7039
ISSN	1083-3021
DOI	10.1007/s10911-023-09552-y
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Article ; Online: Different Regulation of Glut1 Expression and Glucose Uptake during the Induction and Chronic Stages of TGFβ1-Induced EMT in Breast Cancer Cells.

Nilchian, Azadeh / Giotopoulou, Nikolina / Sun, Wenwen / Fuxe, Jonas

Biomolecules

2020 Volume 10, Issue 12

Abstract: Transforming growth factor beta 1 (TGF-β1) is associated with epithelial-mesenchymal transition (EMT), lymph metastasis, and poor prognosis in breast cancer. Paradoxically, TGF-β1 is also a potent inhibitor of cell proliferation. TGF-β1-induced EMT ... ...

Abstract	Transforming growth factor beta 1 (TGF-β1) is associated with epithelial-mesenchymal transition (EMT), lymph metastasis, and poor prognosis in breast cancer. Paradoxically, TGF-β1 is also a potent inhibitor of cell proliferation. TGF-β1-induced EMT involves activation of several pathways including AKT, which also regulates glucose uptake. Recent data show that prolonged TGF-β1 exposure leads to a more stable EMT phenotype in breast cancer cells. However, whether this is linked to changes in glucose metabolism is not clear. Here, we used a model of TGF-β1-induced EMT in mammary epithelial cells to study the regulation of Glut1 and EMT markers during the induction compared to a prolonged phase of EMT by western blot, immunofluorescence and qPCR analysis. We also measured cell proliferation and uptake of the glucose analogue 2-NDBG. We found that EMT induction was associated with decreased Glut1 expression and glucose uptake. These effects were linked to reduced cell proliferation rather than EMT. Knockdown of Glut1 resulted in growth inhibition and less induction of vimentin during TGF-β1-induced EMT. Intriguingly, Glut1 levels, glucose uptake and cell proliferation were restored during prolonged EMT. The results link Glut1 repression to the anti-proliferative response of TGF-β1 and indicate that re-expression of Glut1 during chronic TGF-β1 exposure allows breast cancer cells to develop stable EMT and proliferate, in parallel.
MeSH term(s)	Biological Transport/drug effects ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Epithelial-Mesenchymal Transition/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Glucose/metabolism ; Glucose Transporter Type 1/metabolism ; Humans ; Transforming Growth Factor beta1/pharmacology
Chemical Substances	Glucose Transporter Type 1 ; Transforming Growth Factor beta1 ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-12-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10121621
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Article ; Online: EMT, inflammation and metastasis.

Vincent, C Theresa / Fuxe, Jonas

Seminars in cancer biology

2017 Volume 47, Page(s) 168–169

MeSH term(s)	Epithelial-Mesenchymal Transition/genetics ; Humans ; Inflammation/genetics ; Inflammation/pathology ; Neoplasm Metastasis ; Neoplasms/genetics ; Neoplasms/pathology
Language	English
Publishing date	2017-09-12
Publishing country	England
Document type	Editorial
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2017.09.003
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Article ; Online: Sex dimorphism in the tumor microenvironment - From bench to bedside and back.

He, Fei / Furones, Andrea Rodgers / Landegren, Nils / Fuxe, Jonas / Sarhan, Dhifaf

Seminars in cancer biology

2022 Volume 86, Issue Pt 3, Page(s) 166–179

Abstract: Cancer represents a significant cause of death and suffering in both the developed and developing countries. Key underlying issues in the mortality of cancer are delayed diagnosis and resistance to treatments. However, improvements in biomarkers ... ...

Abstract	Cancer represents a significant cause of death and suffering in both the developed and developing countries. Key underlying issues in the mortality of cancer are delayed diagnosis and resistance to treatments. However, improvements in biomarkers represent one important step that can be taken for alleviating the suffering caused by malignancy. Precision-based medicine is promising for revolutionizing diagnostic and treatment strategies for cancer patients worldwide. Contemporary methods, including various omics and systems biology approaches, as well as advanced digital imaging and artificial intelligence, allow more accurate assessment of tumor characteristics at the patient level. As a result, treatment strategies can be specifically tailored and adapted for individual and/or groups of patients that carry certain tumor characteristics. This includes immunotherapy, which is based on characterization of the immunosuppressive tumor microenvironment (TME) and, more specifically, the presence and activity of immune cell subsets. Unfortunately, while it is increasingly clear that gender strongly affects immune regulation and response, there is a knowledge gap concerning differences in sex-specific immune responses and how these contribute to the immunosuppressive TME and the response to immunotherapy. In fact, sex dimorphism is poorly understood in cancer progression and is typically ignored in current clinical practice. In this review, we aim to survey the available literature and highlight the existing knowledge gap in order to encourage further studies that would contribute to understanding both gender-biased immunosuppression in the TME and the driver of tumor progression towards invasive and metastatic disease. The review highlights the need to include sex optimized/genderized medicine as a new concept in future medicine cancer diagnostics and treatments.
MeSH term(s)	Male ; Female ; Humans ; Tumor Microenvironment ; Sex Characteristics ; Artificial Intelligence ; Immunotherapy/methods ; Neoplasms/diagnosis ; Neoplasms/etiology ; Neoplasms/therapy ; Immunologic Factors
Chemical Substances	Immunologic Factors
Language	English
Publishing date	2022-03-10
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2022.03.007
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Article ; Online: Mapping the Interactome of the Nuclear Heparan Sulfate Proteoglycan Syndecan-1 in Mesothelioma Cells.

Kumar-Singh, Ashish / Shrinet, Jatin / Parniewska, Malgorzata Maria / Fuxe, Jonas / Dobra, Katalin / Hjerpe, Anders

Biomolecules

2020 Volume 10, Issue 7

Abstract: Syndecan-1 (SDC1) is a cell surface heparan sulfate proteoglycan (HSPG), which regulates various signaling pathways controlling the proliferation and migration of malignant mesothelioma and other types of cancer. We have previously shown that SDC1 can ... ...

Abstract	Syndecan-1 (SDC1) is a cell surface heparan sulfate proteoglycan (HSPG), which regulates various signaling pathways controlling the proliferation and migration of malignant mesothelioma and other types of cancer. We have previously shown that SDC1 can translocate to the nucleus in mesothelioma cells through a tubulin-dependent transport mechanism. However, the role of nuclear SDC1 is largely unknown. Here, we performed co-immunoprecipitation (Co-IP) of SDC1 in a mesothelioma cell line to identify SDC1 interacting proteins. The precipitates contained a large number of proteins, indicating the recovery of protein networks. Proteomic analysis with a focus on nuclear proteins revealed an association with pathways related to cell proliferation and RNA synthesis, splicing and transport. In support of this, the top RNA splicing candidates were verified to interact with SDC1 by Co-IP and subsequent Western blot analysis. Further loss- and gain-of-function experiments showed that SDC1 influences RNA levels in mesothelioma cells. The results identify a proteomic map of SDC1 nuclear interactors in a mesothelioma cell line and suggest a previously unknown role for SDC1 in RNA biogenesis. The results should serve as a fundament for further studies to discover the role of nuclear SDC1 in normal and cancer cells of different origin.
MeSH term(s)	Cell Line ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Cell Proliferation ; Gain of Function Mutation ; Gene Expression Regulation, Neoplastic ; Humans ; Loss of Function Mutation ; Mesothelioma/genetics ; Mesothelioma/metabolism ; Protein Interaction Maps ; Proteomics/methods ; RNA Splicing ; Syndecan-1/genetics ; Syndecan-1/metabolism
Chemical Substances	SDC1 protein, human ; Syndecan-1
Language	English
Publishing date	2020-07-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10071034
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Article: Nuclear Syndecan-1 Regulates Epithelial-Mesenchymal Plasticity in Tumor Cells.

Kumar-Singh, Ashish / Parniewska, Malgorzata Maria / Giotopoulou, Nikolina / Javadi, Joman / Sun, Wenwen / Szatmári, Tünde / Dobra, Katalin / Hjerpe, Anders / Fuxe, Jonas

Biology

2021 Volume 10, Issue 6

Abstract: Tumor cells undergoing epithelial-mesenchymal transition (EMT) lose cell surface adhesion molecules and gain invasive and metastatic properties. EMT is a plastic process and tumor cells may shift between different epithelial-mesenchymal states during ... ...

Abstract	Tumor cells undergoing epithelial-mesenchymal transition (EMT) lose cell surface adhesion molecules and gain invasive and metastatic properties. EMT is a plastic process and tumor cells may shift between different epithelial-mesenchymal states during metastasis. However, how this is regulated is not fully understood. Syndecan-1 (SDC1) is the major cell surface proteoglycan in epithelial cells and has been shown to regulate carcinoma progression and EMT. Recently, it was discovered that SDC1 translocates into the cell nucleus in certain tumor cells. Nuclear SDC1 inhibits cell proliferation, but whether nuclear SDC1 contributes to the regulation of EMT is not clear. Here, we report that loss of nuclear SDC1 is associated with cellular elongation and an E-cadherin-to-N-cadherin switch during TGF-β1-induced EMT in human A549 lung adenocarcinoma cells. Further studies showed that nuclear translocation of SDC1 contributed to the repression of mesenchymal and invasive properties of human B6FS fibrosarcoma cells. The results demonstrate that nuclear translocation contributes to the capacity of SDC1 to regulate epithelial-mesenchymal plasticity in human tumor cells and opens up to mechanistic studies to elucidate the mechanisms involved.
Language	English
Publishing date	2021-06-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology10060521
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Article ; Online: Nuclear Syndecan-1 Regulates Epithelial-Mesenchymal Plasticity in Tumor Cells

Ashish Kumar-Singh / Malgorzata Maria Parniewska / Nikolina Giotopoulou / Joman Javadi / Wenwen Sun / Tünde Szatmári / Katalin Dobra / Anders Hjerpe / Jonas Fuxe

Biology, Vol 10, Iss 521, p

2021 Volume 521

Abstract	Tumor cells undergoing epithelial-mesenchymal transition (EMT) lose cell surface adhesion molecules and gain invasive and metastatic properties. EMT is a plastic process and tumor cells may shift between different epithelial-mesenchymal states during metastasis. However, how this is regulated is not fully understood. Syndecan-1 (SDC1) is the major cell surface proteoglycan in epithelial cells and has been shown to regulate carcinoma progression and EMT. Recently, it was discovered that SDC1 translocates into the cell nucleus in certain tumor cells. Nuclear SDC1 inhibits cell proliferation, but whether nuclear SDC1 contributes to the regulation of EMT is not clear. Here, we report that loss of nuclear SDC1 is associated with cellular elongation and an E-cadherin-to-N-cadherin switch during TGF-β1-induced EMT in human A549 lung adenocarcinoma cells. Further studies showed that nuclear translocation of SDC1 contributed to the repression of mesenchymal and invasive properties of human B6FS fibrosarcoma cells. The results demonstrate that nuclear translocation contributes to the capacity of SDC1 to regulate epithelial-mesenchymal plasticity in human tumor cells and opens up to mechanistic studies to elucidate the mechanisms involved.
Keywords	syndecan-1 ; SDC1 ; nuclear translocation ; epithelial-mesenchymal transition ; plasticity ; TGF-β1 ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Epithelial-mesenchymal transition in cancer metastasis through the lymphatic system.

Karlsson, Mikael C / Gonzalez, Santiago F / Welin, Josefin / Fuxe, Jonas

Molecular oncology

2017 Volume 11, Issue 7, Page(s) 781–791

Abstract: It was already in the 18th century when the French surgeon LeDran first noted that breast cancer patients with spread of tumor cells to their axillary lymph nodes had a drastically worse prognosis than patients without spread (LeDran et al., ). Since ... ...

Abstract	It was already in the 18th century when the French surgeon LeDran first noted that breast cancer patients with spread of tumor cells to their axillary lymph nodes had a drastically worse prognosis than patients without spread (LeDran et al., ). Since then, metastatic spread of cancer cells to regional lymph nodes has been established as the most important prognostic factor in many types of cancer (Carter et al., Elston and Ellis, ). However, despite its clinical importance, lymph metastasis remains an underexplored area of tumor biology. Fundamental questions, such as when, how, and perhaps most importantly, why tumor cells disseminate through the lymphatic system, remain largely unanswered. Accordingly, no treatment strategies exist that specifically target lymph metastasis. The identification of epithelial-mesenchymal transition (EMT) as a mechanism, which allows cancer cells to dedifferentiate and acquire enhanced migratory and invasive properties, has been a game changer in cancer research. Conceptually, EMT provides an explanation for why epithelial cancers with poor differentiation status are generally more aggressive and prone to metastasize than more differentiated cancers. Inflammatory cytokines, such as TGF-β, which are produced and secreted by tumor-infiltrating immune cells, are potent inducers of EMT. Thus, reactivation of EMT also links cancer-related inflammation to invasive and metastatic disease. Recently, we found that breast cancer cells undergoing TGF-β-induced EMT acquire properties of immune cells allowing them to disseminate in a targeted fashion through the lymphatic system similar to activated dendritic cells during inflammation. Here, we review our current understanding of the mechanisms by which cancer cells spread through the lymphatic system and the links to inflammation and the immune system. We also emphasize how imaging techniques have the potential to further expand our knowledge of the mechanisms of lymph metastasis, and how lymph nodes serve as an interface between cancer and the immune system.
MeSH term(s)	Animals ; Epithelial-Mesenchymal Transition/immunology ; Humans ; Lymph Nodes/immunology ; Lymph Nodes/pathology ; Lymphatic Metastasis ; Neoplasm Proteins/immunology ; Neoplasms/immunology ; Neoplasms/pathology ; Transforming Growth Factor beta/immunology
Chemical Substances	Neoplasm Proteins ; Transforming Growth Factor beta
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1002/1878-0261.12092
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Zs.A 6637: Show issues

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Article ; Online: TGF-β-induced epithelial-mesenchymal transition: a link between cancer and inflammation.

Fuxe, Jonas / Karlsson, Mikael C I

Seminars in cancer biology

2012 Volume 22, Issue 5-6, Page(s) 455–461

Abstract: Metastatic spread of tumor cells to vital organs is the major cause of death in cancer. Accumulating data support an important role of infiltrating immune cells in promoting carcinoma progression into metastatic disease. Tumor-infiltrating immune cells ... ...

Abstract	Metastatic spread of tumor cells to vital organs is the major cause of death in cancer. Accumulating data support an important role of infiltrating immune cells in promoting carcinoma progression into metastatic disease. Tumor-infiltrating immune cells produce and secrete cytokines, growth factors and proteases that re-activate latent developmental processes including epithelial-mesenchymal transition (EMT). EMT provides tumor cells with invasive, migratory and stem cell properties allowing them to disseminate and propagate at distant sites. Induction of EMT requires two criteria to be fulfilled: (i) cells are competent to undergo EMT (ii) an EMT-permissive microenvironment exists. The cytokine TGF-β, which is expressed by tumor-infiltrating immune cells, stands out as a master regulator of the pro-invasive tumor microenvironment. TGF-β cooperates with stem cell pathways, such as Wnt and Ras signaling, to induce EMT. In addition, TGF-β contributes to an EMT-permissive microenvironment by switching the phenotypes of tumor-infiltrating immune cells, which thereby mount pro-invasive and pro-metastatic immune responses. In this review, we discuss the role of TGF-β-induced EMT as a link between cancer and inflammation in the context of questions, which from our point of view are key to answer in order to understand the functionality of EMT in tumors.
MeSH term(s)	Animals ; Cell Movement/immunology ; Cytokines/immunology ; Cytokines/metabolism ; Epithelial-Mesenchymal Transition ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta/metabolism ; Tumor Microenvironment/immunology
Chemical Substances	Cytokines ; Transforming Growth Factor beta
Language	English
Publishing date	2012-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2012.05.004
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Article ; Online: Induction of the Coxsackievirus and Adenovirus Receptor in Macrophages During the Formation of Atherosclerotic Plaques.

Nilchian, Azadeh / Plant, Estelle / Parniewska, Malgorzata M / Santiago, Ana / Rossignoli, Aránzazu / Skogsberg, Josefin / Hedin, Ulf / Matic, Ljubica / Fuxe, Jonas

The Journal of infectious diseases

2020 Volume 222, Issue 12, Page(s) 2041–2051

Abstract: Multiple viruses are implicated in atherosclerosis, but the mechanisms by which they infect cells and contribute to plaque formation in arterial walls are not well understood. Based on reports showing the presence of enterovirus in atherosclerotic ... ...

Abstract	Multiple viruses are implicated in atherosclerosis, but the mechanisms by which they infect cells and contribute to plaque formation in arterial walls are not well understood. Based on reports showing the presence of enterovirus in atherosclerotic plaques we hypothesized that the coxsackievirus and adenovirus receptor (CXADR/CAR), although absent in normal arteries, could be induced during plaque formation. Large-scale microarray and mass spectrometric analyses revealed significant up-regulation of CXADR messenger RNA and protein levels in plaque-invested carotid arteries compared with control arteries. Macrophages were identified as a previously unknown cellular source of CXADR in human plaques and plaques from Ldr-/-Apob100/100 mice. CXADR was specifically associated with M1-polarized macrophages and foam cells and was experimentally induced during macrophage differentiation. Furthermore, it was significantly correlated with receptors for other viruses linked to atherosclerosis. The results show that CXADR is induced in macrophages during plaque formation, suggesting a mechanism by which enterovirus infect cells in atherosclerotic plaques.
MeSH term(s)	Animals ; Carotid Arteries/virology ; Coxsackie and Adenovirus Receptor-Like Membrane Protein/metabolism ; Disease Models, Animal ; Enterovirus/pathogenicity ; Humans ; Macrophages/metabolism ; Macrophages/virology ; Mice ; Mice, Knockout ; Plaque, Atherosclerotic/metabolism ; Plaque, Atherosclerotic/virology ; RNA, Messenger/metabolism
Chemical Substances	CLMP protein, human ; Coxsackie and Adenovirus Receptor-Like Membrane Protein ; RNA, Messenger
Language	English
Publishing date	2020-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiaa418
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