Research ExplorerPublicationsAngiotensin Inhibition, TGF-β and EMT in Cancer

Angiotensin Inhibition, TGF-β and EMT in Cancer

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Angiotensin Inhibition, TGF-β and EMT in Cancer. / Pallasch, Fabian Bernhard; Schumacher, Udo.

In: CANCERS, Vol. 12, No. 10, 28.09.2020.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Pallasch, FB & Schumacher, U 2020, 'Angiotensin Inhibition, TGF-β and EMT in Cancer', CANCERS, vol. 12, no. 10. https://doi.org/10.3390/cancers12102785

APA

Pallasch, F. B., & Schumacher, U. (2020). Angiotensin Inhibition, TGF-β and EMT in Cancer. CANCERS, 12(10). https://doi.org/10.3390/cancers12102785

Vancouver

Pallasch FB, Schumacher U. Angiotensin Inhibition, TGF-β and EMT in Cancer. CANCERS. 2020 Sep 28;12(10). https://doi.org/10.3390/cancers12102785

Bibtex

@article{58c898f4756b4823bb97be85c3e3510c,
title = "Angiotensin Inhibition, TGF-β and EMT in Cancer",
abstract = "Angiotensin inhibitors are standard drugs in cardiovascular and renal diseases that have antihypertensive and antifibrotic properties. These drugs also exert their antifibrotic effects in cancer by reducing collagen and hyaluronan deposition in the tumor stroma, thus enhancing drug delivery. Angiotensin II signaling interferes with the secretion of the cytokine TGF-β-a known driver of malignancy. TGF-β stimulates matrix production in cancer-associated fibroblasts, and thus drives desmoplasia. The effect of TGF-β on cancer cells itself is stage-dependent and changes during malignant progression from inhibitory to stimulatory. The intracellular signaling for the TGF-β family can be divided into an SMAD-dependent canonical pathway and an SMAD-independent noncanonical pathway. These capabilities have made TGF-β an interesting target for numerous drug developments. TGF-β is also an inducer of epithelial-mesenchymal transition (EMT). EMT is a highly complex spatiotemporal-limited process controlled by a plethora of factors. EMT is a hallmark of metastatic cancer, and with its reversal, an important step in the metastatic cascade is characterized by a loss of epithelial characteristics and/or the gain of mesenchymal traits.",
author = "Pallasch, {Fabian Bernhard} and Udo Schumacher",
year = "2020",
month = sep,
day = "28",
doi = "10.3390/cancers12102785",
language = "English",
volume = "12",
journal = "CANCERS",
issn = "2072-6694",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "10",

}

RIS

TY - JOUR

T1 - Angiotensin Inhibition, TGF-β and EMT in Cancer

AU - Pallasch, Fabian Bernhard

AU - Schumacher, Udo

PY - 2020/9/28

Y1 - 2020/9/28

N2 - Angiotensin inhibitors are standard drugs in cardiovascular and renal diseases that have antihypertensive and antifibrotic properties. These drugs also exert their antifibrotic effects in cancer by reducing collagen and hyaluronan deposition in the tumor stroma, thus enhancing drug delivery. Angiotensin II signaling interferes with the secretion of the cytokine TGF-β-a known driver of malignancy. TGF-β stimulates matrix production in cancer-associated fibroblasts, and thus drives desmoplasia. The effect of TGF-β on cancer cells itself is stage-dependent and changes during malignant progression from inhibitory to stimulatory. The intracellular signaling for the TGF-β family can be divided into an SMAD-dependent canonical pathway and an SMAD-independent noncanonical pathway. These capabilities have made TGF-β an interesting target for numerous drug developments. TGF-β is also an inducer of epithelial-mesenchymal transition (EMT). EMT is a highly complex spatiotemporal-limited process controlled by a plethora of factors. EMT is a hallmark of metastatic cancer, and with its reversal, an important step in the metastatic cascade is characterized by a loss of epithelial characteristics and/or the gain of mesenchymal traits.

AB - Angiotensin inhibitors are standard drugs in cardiovascular and renal diseases that have antihypertensive and antifibrotic properties. These drugs also exert their antifibrotic effects in cancer by reducing collagen and hyaluronan deposition in the tumor stroma, thus enhancing drug delivery. Angiotensin II signaling interferes with the secretion of the cytokine TGF-β-a known driver of malignancy. TGF-β stimulates matrix production in cancer-associated fibroblasts, and thus drives desmoplasia. The effect of TGF-β on cancer cells itself is stage-dependent and changes during malignant progression from inhibitory to stimulatory. The intracellular signaling for the TGF-β family can be divided into an SMAD-dependent canonical pathway and an SMAD-independent noncanonical pathway. These capabilities have made TGF-β an interesting target for numerous drug developments. TGF-β is also an inducer of epithelial-mesenchymal transition (EMT). EMT is a highly complex spatiotemporal-limited process controlled by a plethora of factors. EMT is a hallmark of metastatic cancer, and with its reversal, an important step in the metastatic cascade is characterized by a loss of epithelial characteristics and/or the gain of mesenchymal traits.

U2 - 10.3390/cancers12102785

DO - 10.3390/cancers12102785

M3 - SCORING: Review article

C2 - 32998363

VL - 12

JO - CANCERS

JF - CANCERS

SN - 2072-6694

IS - 10

ER -