scholarly journals Transforming Growth Factor-β: A Multifunctional Regulator of Cancer Immunity

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3099
Author(s):  
Vivian Weiwen Xue ◽  
Jeff Yat-Fai Chung ◽  
Cristina Alexandra García Córdoba ◽  
Alvin Ho-Kwan Cheung ◽  
Wei Kang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cancer Progression ◽  
Transforming Growth Factor ◽  
Molecular Level ◽  
Transforming Growth Factor Β ◽  
Tumour Microenvironment ◽  
Cell Type ◽  
Cancer Immunity ◽  
Canonical Pathways ◽  
Cell Type Specific

Transforming growth factor-β (TGF-β) was originally identified as an anti-tumour cytokine. However, there is increasing evidence that it has important roles in the tumour microenvironment (TME) in facilitating cancer progression. TGF-β actively shapes the TME via modulating the host immunity. These actions are highly cell-type specific and complicated, involving both canonical and non-canonical pathways. In this review, we systemically update how TGF-β signalling acts as a checkpoint regulator for cancer immunomodulation. A better appreciation of the underlying pathogenic mechanisms at the molecular level can lead to the discovery of novel and more effective therapeutic strategies for cancer.

scholarly journals SnoN Is a Cell Type-specific Mediator of Transforming Growth Factor-β Responses

2005 ◽  
Vol 280 (13) ◽  
pp. 13037-13046 ◽  
Author(s):  
Krishna P. Sarker ◽  
Sylvia M. Wilson ◽  
Shirin Bonni
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cell Type ◽  
A Cell ◽  
Cell Type Specific

scholarly journals Cell Type-Specific Expression of Transforming Growth Factor-β 1 in the Mouse Uterus during the Periimplantation Period

1990 ◽  
Vol 4 (7) ◽  
pp. 965-972 ◽  
Author(s):  
Hiromichi Tamada ◽  
Michael T. McMaster ◽  
Kathleen C. Flanders ◽  
Glen K. Andrews ◽  
Sudhansu K. Dey
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cell Type ◽  
Mouse Uterus ◽  
Specific Expression ◽  
Cell Type Specific Expression ◽  
Cell Type Specific

The human NUPR1/P8 gene is transcriptionally activated by transforming growth factor β via the SMAD signalling pathway

2012 ◽  
Vol 445 (2) ◽  
pp. 285-293 ◽  
Author(s):  
Roxane M. Pommier ◽  
Johann Gout ◽  
David F. Vincent ◽  
Carla E. Cano ◽  
Bastien Kaniewski ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cancer Progression ◽  
Stress Resistance ◽  
Nuclear Protein ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Transcriptional Level ◽  
Smad Proteins ◽  
Activation Cascade ◽  
Tgfβ Superfamily

NUPR1 (nuclear protein 1), also called P8 (molecular mass 8 kDa) or COM1 (candidate of metastasis 1), is involved in the stress response and in cancer progression. In the present study, we investigated whether human NUPR1 expression was regulated by TGFβ (transforming growth factor β), a secreted polypeptide largely involved in tumorigenesis. We demonstrate that the expression of NUPR1 was activated by TGFβ at the transcriptional level. We show that this activation is mediated by the SMAD proteins, which are transcription factors specifically involved in the signalling of TGFβ superfamily members. NUPR1 promoter analysis reveals the presence of a functional TGFβ-response element binding the SMAD proteins located in the genomic DNA region corresponding to the 5′-UTR (5′-untranslated region). Altogether, the molecular results of the present study, which demonstrate the existence of a TGFβ/SMAD/NUPR1 activation cascade, open the way to consider and investigate further a new mechanism enabling TGFβ to promote tumorigenesis by inducing stress resistance.

scholarly journals Alteration in transforming growth factor-β receptor expression in gallbladder disease: implications of chronic cholelithiasis and chronic Salmonella typhi infection

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Yogesh D. Walawalkar ◽  
Yatindra Vaidya ◽  
Vijayashree Nayak
Keyword(s):  
Growth Factor ◽  
Cancer Progression ◽  
Transforming Growth Factor ◽  
Receptor Gene ◽  
Gallbladder Disease ◽  
Fold Increase ◽  
Transforming Growth Factor Β ◽  
Salmonella Typhi ◽  
Receptor Expression ◽  
Β Receptor

Gallbladder cancer prevalence is ever increasing with <em>Salmonella typhi</em> chronic infection being one of the predisposing factors. Altered ratios or expression of transforming growth factor-β (TGF-β) receptors and changes in its function are associated with loss in anti-proliferative effects of TGF-β and cancer progression. Using reverse transcriptase polymerase chain reaction we monitor any changes in TGF-β receptor gene expression. We simultaneously screen for <em>S. typhi</em> within the samples. From 73 patients undergoing cholecystectomy 39-50% had significant expression (P&lt;0.05) of TGF-β receptor (TβR)- I and TβR-II during chronic cholelithiasis as compared to the remaining 19-23% with acute chronic cholelithiasis. There was no significant increase in TβR-III receptor expression. Patient’s positive for <em>S. typhi</em> (7/73) did not show any significant changes in expression of these receptors, thus indicating no direct relation in regulating the host TGFβ-signaling pathway. Further analysis on expression of downstream Smad components revealed that patients with up-regulated TGFβ receptor expression show &gt;2-fold increase in the RSmads and Co-Smads with a &gt;2-fold decrease in I-Smads. Thus gain of TβR-I and II expression in epithelial cells of the gallbladder was associated with chronic inflammatory stages of the gallbladder disease.

scholarly journals Transforming Growth Factor-β Signaling in Fibrotic Diseases and Cancer-Associated Fibroblasts

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1666
Author(s):  
Xueke Shi ◽  
Christian D. Young ◽  
Hongmei Zhou ◽  
Xiao-Jing Wang
Keyword(s):  
Growth Factor ◽  
Cancer Progression ◽  
Immune Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cell Types ◽  
Cancer Associated Fibroblasts ◽  
The Matrix ◽  
Fibrotic Diseases ◽  
Fibrotic Disorders

Transforming growth factor-β (TGF-β) signaling is essential in embryo development and maintaining normal homeostasis. Extensive evidence shows that TGF-β activation acts on several cell types, including epithelial cells, fibroblasts, and immune cells, to form a pro-fibrotic environment, ultimately leading to fibrotic diseases. TGF-β is stored in the matrix in a latent form; once activated, it promotes a fibroblast to myofibroblast transition and regulates extracellular matrix (ECM) formation and remodeling in fibrosis. TGF-β signaling can also promote cancer progression through its effects on the tumor microenvironment. In cancer, TGF-β contributes to the generation of cancer-associated fibroblasts (CAFs) that have different molecular and cellular properties from activated or fibrotic fibroblasts. CAFs promote tumor progression and chronic tumor fibrosis via TGF-β signaling. Fibrosis and CAF-mediated cancer progression share several common traits and are closely related. In this review, we consider how TGF-β promotes fibrosis and CAF-mediated cancer progression. We also discuss recent evidence suggesting TGF-β inhibition as a defense against fibrotic disorders or CAF-mediated cancer progression to highlight the potential implications of TGF-β-targeted therapies for fibrosis and cancer.

Regeneration neurohormones and growth factors in echinoderms

2001 ◽  
Vol 79 (7) ◽  
pp. 1171-1208 ◽  
Author(s):  
M C Thorndyke ◽  
MD Candia Carnevali
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Molecular Level ◽  
Distribution Patterns ◽  
Transforming Growth Factor Β ◽  
Regenerative Processes ◽  
Blastema Formation ◽  
Undifferentiated Cells ◽  
Growth Promoting

There has been much recent interest in the presence and biological functions of growth regulators in invertebrates. In spite of the different distribution patterns of these molecules in different phyla (from molluscs, insects, and annelids to echinoderms and tunicates), they seem always to be extensively involved in developmental processes, both embryonic and regenerative. Echinoderms are well known for their striking regenerative potential and many can completely regenerate arms that, for example, are lost following self-induced or traumatic amputation. Thus, they provide a valuable experimental model for the study of regenerative processes from the macroscopic to the molecular level. In crinoids as well as probably all ophiuroids, regeneration is rapid and occurs by means of a mechanism that involves blastema formation, known as epimorphosis, where the new tissues arise from undifferentiated cells. In asteroids, morphallaxis is the mechanism employed, replacement cells being derived from existing tissues following differentiation and (or) transdifferentiation. This paper focuses on the possible contribution of neurohormones and growth factors during both repair and regenerative processes. Three different classes of regulatory molecules are proposed as plausible candidates for growth-promoting factors in regeneration: neurotransmitters (monoamines), neuropeptides (substance P, SALMFamides 1 and 2), and growth-factor-like molecules (TGF-β (transforming growth factor β), NGF (nerve growth factor), RGF-2 (basic fibroblast growth factor)).

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