Migration Stimulating Factor (MSF): Its Role in the Tumour
Microenvironment

C 2021

Migration Stimulating Factor (MSF): Its Role in the Tumour Microenvironment

SCHOR, A. M., A. M. WOOLSTON, Kateřina KAŇKOVÁ, K. HARADA, L. E. ALJORANI et. al.

Základní údaje

Originální název

Migration Stimulating Factor (MSF): Its Role in the Tumour Microenvironment

Autoři

SCHOR, A. M., A. M. WOOLSTON, Kateřina KAŇKOVÁ (203 Česká republika, domácí), K. HARADA, L. E. ALJORANI, S. PERRIER, P. A. FELTS, R. P. KEATCH a S. L. SCHOR

Vydání

Neuveden, Tumor Microenvironment: Novel Concepts, od s. 351-397, 47 s. Advances in Experimental Medicine and Biology, Volume 1329, 2021

Nakladatel

Springer

Další údaje

Jazyk

angličtina

Typ výsledku

Kapitola resp. kapitoly v odborné knize

Obor

30109 Pathology

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Forma vydání

tištěná verze "print"

Odkazy

URL

Kód RIV

RIV/00216224:14110/21:00123828

Organizační jednotka

Lékařská fakulta

ISBN

978-3-030-73118-2

DOI

http://dx.doi.org/10.1007/978-3-030-73119-9_18

UT WoS

000753882600019

Klíčová slova anglicky

Migration Stimulating Factor (MSF); Fibronectin isoforms; Oncofoetal protein; Cancer-associated fibroblasts (CAF); Sprouting (angiogenic) endothelial cells; Tumour cells; Macrophages IGD peptides; TGFβ1; NGAL; IGFBP-7; Cell migration; Angiogenesis

Štítky

rivok, topvydavatel

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 17. 5. 2022 12:54, Mgr. Tereza Miškechová

Anotace

V originále

Migration Stimulating Factor (MSF) is a 70 kDa truncated isoform of fibronectin (FN); its mRNA is generated from the FN gene by an unusual two-stage processing. Unlike full-length FN, MSF is not a matrix molecule but a soluble protein which displays cytokine-like activities not displayed by any other FN isoform due to steric hindrance. There are two isoforms of MSF; these are referred to as MSF+aa and MSF-aa, while the term MSF is used to include both. MSF was first identified as a motogen secreted by foetal and cancer-associated fibroblasts in tissue culture. It is also produced by sprouting (angiogenic) endothelial cells, tumour cells and activated macrophages. Keratinocytes and resting endothelial cells secrete inhibitors of MSF that have been identified as NGAL and IGFBP-7, respectively. MSF+aa and MSF-aa show distinct functionality in that only MSF+aa is inhibited by NGAL. MSF is present in 70–80% of all tumours examined, expressed by the tumour cells as well as by fibroblasts, endothelial cells and macrophages in the tumour microenvironment (TME). High MSF expression is associated with tumour progression and poor prognosis in all tumours examined, including breast carcinomas, non-small cell lung cancer (NSCLC), salivary gland tumours (SGT) and oral squamous cell carcinomas (OSCC). Epithelial and stromal MSF carry independent prognostic value. MSF is also expressed systemically in cancer patients, being detected in serum and produced by fibroblast from distal uninvolved skin. MSF-aa is the main isoform associated with cancer, whereas MSF+aa may be expressed by both normal and malignant tissues. The expression of MSF is not invariant; it may be switched on and off in a reversible manner, which requires precise interactions between soluble factors present in the TME and the extracellular matrix in contact with the cells. MSF expression in fibroblasts may be switched on by a transient exposure to several molecules, including TGFβ1 and MSF itself, indicating an auto-inductive capacity. Acting by both paracrine and autocrine mechanisms, MSF stimulates cell migration/invasion, induces angiogenesis and cell differentiation and alters the matrix and cellular composition of the TME. MSF is also a survival factor for sprouting endothelial cells. IGD tri- and tetra-peptides mimic the motogenic and angiogenic activities of MSF, with both molecules inhibiting AKT activity and requiring αvβ3 functionality. MSF is active at unprecedently low concentrations in a manner which is target cell specific. Thus, different bioactive motifs and extracellular matrix requirements apply to fibroblasts, endothelial cells and tumour cells. Unlike other motogenic and angiogenic factors, MSF does not affect cell proliferation but it stimulates tumour growth through its angiogenic effect and downstream mechanisms. The epithelial-stromal pattern of expression and range of bioactivities displayed puts MSF in the unique position of potentially promoting tumour progression from both the “seed” and the “soil” perspectives.

Citovat

SCHOR, A. M., A. M. WOOLSTON, Kateřina KAŇKOVÁ, K. HARADA, L. E. ALJORANI, S. PERRIER, P. A. FELTS, R. P. KEATCH a S. L. SCHOR. Migration Stimulating Factor (MSF): Its Role in the Tumour Microenvironment. In Alexander Birbrair. Tumor Microenvironment: Novel Concepts. Neuveden: Springer, 2021, s. 351-397. Advances in Experimental Medicine and Biology, Volume 1329. ISBN 978-3-030-73118-2. Dostupné z: https://dx.doi.org/10.1007/978-3-030-73119-9_18.

@inbook{1823809,
   author = {Schor, A. M. and Woolston, A. M. and Kaňková, Kateřina and Harada, K. and Aljorani, L. E. and Perrier, S. and Felts, P. A. and Keatch, R. P. and Schor, S. L.},
   address = {Neuveden},
   booktitle = {Tumor Microenvironment: Novel Concepts},
   doi = {http://dx.doi.org/10.1007/978-3-030-73119-9_18},
   editor = {Alexander Birbrair},
   keywords = {Migration Stimulating Factor (MSF); Fibronectin isoforms; Oncofoetal protein; Cancer-associated fibroblasts (CAF); Sprouting (angiogenic) endothelial cells; Tumour cells; Macrophages IGD peptides; TGFβ1; NGAL; IGFBP-7; Cell migration; Angiogenesis},
   howpublished = {tištěná verze "print"},
   language = {eng},
   location = {Neuveden},
   isbn = {978-3-030-73118-2},
   pages = {351-397},
   publisher = {Springer},
   title = {Migration Stimulating Factor (MSF): Its Role in the Tumour Microenvironment},
   url = {https://link.springer.com/chapter/10.1007%2F978-3-030-73119-9_18},
   year = {2021}
}

TY  - CHAP
ID  - 1823809
AU  - Schor, A. M. - Woolston, A. M. - Kaňková, Kateřina - Harada, K. - Aljorani, L. E. - Perrier, S. - Felts, P. A. - Keatch, R. P. - Schor, S. L.
PY  - 2021
TI  - Migration Stimulating Factor (MSF): Its Role in the Tumour Microenvironment
VL  - Advances in Experimental Medicine and Biology, Volume 1329
PB  - Springer
CY  - Neuveden
SN  - 9783030731182
KW  - Migration Stimulating Factor (MSF)
KW  - Fibronectin isoforms
KW  - Oncofoetal protein
KW  - Cancer-associated fibroblasts (CAF)
KW  - Sprouting (angiogenic) endothelial cells
KW  - Tumour cells
KW  - Macrophages IGD peptides
KW  - TGFβ1
KW  - NGAL
KW  - IGFBP-7
KW  - Cell migration
KW  - Angiogenesis
UR  - https://link.springer.com/chapter/10.1007%2F978-3-030-73119-9_18
N2  - Migration Stimulating Factor (MSF) is a 70 kDa truncated isoform of fibronectin (FN); its mRNA is generated from the FN gene by an unusual two-stage processing. Unlike full-length FN, MSF is not a matrix molecule but a soluble protein which displays cytokine-like activities not displayed by any other FN isoform due to steric hindrance. There are two isoforms of MSF; these are referred to as MSF+aa and MSF-aa, while the term MSF is used to include both. MSF was first identified as a motogen secreted by foetal and cancer-associated fibroblasts in tissue culture. It is also produced by sprouting (angiogenic) endothelial cells, tumour cells and activated macrophages. Keratinocytes and resting endothelial cells secrete inhibitors of MSF that have been identified as NGAL and IGFBP-7, respectively. MSF+aa and MSF-aa show distinct functionality in that only MSF+aa is inhibited by NGAL. MSF is present in 70–80% of all tumours examined, expressed by the tumour cells as well as by fibroblasts, endothelial cells and macrophages in the tumour microenvironment (TME). High MSF expression is associated with tumour progression and poor prognosis in all tumours examined, including breast carcinomas, non-small cell lung cancer (NSCLC), salivary gland tumours (SGT) and oral squamous cell carcinomas (OSCC). Epithelial and stromal MSF carry independent prognostic value. MSF is also expressed systemically in cancer patients, being detected in serum and produced by fibroblast from distal uninvolved skin. MSF-aa is the main isoform associated with cancer, whereas MSF+aa may be expressed by both normal and malignant tissues. The expression of MSF is not invariant; it may be switched on and off in a reversible manner, which requires precise interactions between soluble factors present in the TME and the extracellular matrix in contact with the cells. MSF expression in fibroblasts may be switched on by a transient exposure to several molecules, including TGFβ1 and MSF itself, indicating an auto-inductive capacity. Acting by both paracrine and autocrine mechanisms, MSF stimulates cell migration/invasion, induces angiogenesis and cell differentiation and alters the matrix and cellular composition of the TME. MSF is also a survival factor for sprouting endothelial cells. IGD tri- and tetra-peptides mimic the motogenic and angiogenic activities of MSF, with both molecules inhibiting AKT activity and requiring αvβ3 functionality. MSF is active at unprecedently low concentrations in a manner which is target cell specific. Thus, different bioactive motifs and extracellular matrix requirements apply to fibroblasts, endothelial cells and tumour cells. Unlike other motogenic and angiogenic factors, MSF does not affect cell proliferation but it stimulates tumour growth through its angiogenic effect and downstream mechanisms. The epithelial-stromal pattern of expression and range of bioactivities displayed puts MSF in the unique position of potentially promoting tumour progression from both the “seed” and the “soil” perspectives.
ER  -

SCHOR, A. M., A. M. WOOLSTON, Kateřina KAŇKOVÁ, K. HARADA, L. E. ALJORANI, S. PERRIER, P. A. FELTS, R. P. KEATCH a S. L. SCHOR. Migration Stimulating Factor (MSF): Its Role in the Tumour Microenvironment. In Alexander Birbrair. \textit{Tumor Microenvironment: Novel Concepts}. Neuveden: Springer, 2021, s.~351-397. Advances in Experimental Medicine and Biology, Volume 1329. ISBN~978-3-030-73118-2. Dostupné z: https://dx.doi.org/10.1007/978-3-030-73119-9\_{}18.

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