TGF-β1 Induces EMT in Bovine Mammary Epithelial Cells Through the TGFβ1/Smad Signaling Pathway

Chen, Qing; Yang, Wei; Wang, Xixi; Li, Xueru; Qi, Shao-pei; Zhang, Yong; Gao, Ming-Qing

doi:10.1159/000480321

Cited by 57 publications

(60 citation statements)

References 43 publications

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“…We have shown that TGF-b1 introduces EMT by the classical TGF-b1/Smad pathway in bovine mammary epithelial cells [20]. In this study, higher mRNA level ( Fig.…”

Section: Knockout Of Lncrna-tub Caused Lower Tuba1c and Higher Tgf-b1supporting

confidence: 59%

A novel long non‐coding RNA regulates the immune response in MAC‐T cells and contributes to bovine mastitis

Wang

et al. 2019

The FEBS Journal

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The long non‐coding RNAs (lncRNAs) are known to transcriptionally regulate a wide spectrum of diseases. Here, we screened for potentially functional lncRNAs in a mammary epithelial cell model of bovine mastitis by RNA‐Seq technology and identified a class of previously undetected mastitis‐related lncRNAs. A novel lncRNA was widely expressed in a variety of bovine tissues with diverse relative abundance and had a relatively low expression in mammary tissue. Given its predicted target gene is TUBA1C, we name it lncRNA‐TUB. We found a higher expression of lncRNA‐TUB in mammary epithelial cells that received a proinflammatory stimulus compared to normal cells. Knockout of lncRNA‐TUB by the CRISPR/Cas9 system revealed that it plays crucial roles in the morphological shape, proliferation, migration and β‐casein secretion of mammary epithelial cells. In addition, lncRNA‐TUB mediates Escherichia coli‐induced inflammatory factor secretion and Staphylococcus aureus adhesion to epithelial cells. Our results suggest that the lncRNAs identified here function in bovine mastitis, and that lncRNA‐TUB affects the basic biological characteristics and functions of bovine mammary epithelial cells in inflammatory conditions, providing valuable insights into the mechanisms of bovine mastitis.

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“…We have shown that TGF-b1 introduces EMT by the classical TGF-b1/Smad pathway in bovine mammary epithelial cells [20]. In this study, higher mRNA level ( Fig.…”

Section: Knockout Of Lncrna-tub Caused Lower Tuba1c and Higher Tgf-b1supporting

confidence: 59%

A novel long non‐coding RNA regulates the immune response in MAC‐T cells and contributes to bovine mastitis

Wang

et al. 2019

The FEBS Journal

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“…Studies have shown that EMT is closely related to invasion and migration in bladder cancer. 15 Thus, we further explored whether starvation-induced autophagy promoted EMT through the TGF-β/Smad signaling pathway. The epithelial marker E-cadherin was significantly expressed in the control group, CQ-only group, and 3MA-only group.…”

Section: Starvation-induced Autophagy Promotes the Invasion And Migmentioning

confidence: 99%

“…15 TGF-β1 is an extracellular membrane ligand that binds to the membrane-type TGF-β receptor II and activates TGF-β receptor I. TGF-β receptor I phosphorylates Smad2 and Smad3, further forming a complex with Smad4 and entering the nucleus to bind with other DNAbinding factors such as Snail, ZEB, and Twist to induce EMT. 15 TGF-β1 is an extracellular membrane ligand that binds to the membrane-type TGF-β receptor II and activates TGF-β receptor I. TGF-β receptor I phosphorylates Smad2 and Smad3, further forming a complex with Smad4 and entering the nucleus to bind with other DNAbinding factors such as Snail, ZEB, and Twist to induce EMT.…”

Section: F I G U R E 3 Autophagy Promotes the Invasion And Migration mentioning

confidence: 99%

“…11 It has been shown that EMT is closely associated with the invasion and migration of bladder cancer. 14,15 It has been demonstrated that starvation-induced autophagy promotes EMT in hepatocellular carcinoma through the TGF-β/Smad3 signaling pathway, 16 and TGF-β1 also upregulates autophagy-related proteins to promote autophagy. 14,15 It has been demonstrated that starvation-induced autophagy promotes EMT in hepatocellular carcinoma through the TGF-β/Smad3 signaling pathway, 16 and TGF-β1 also upregulates autophagy-related proteins to promote autophagy.…”

Section: Introductionmentioning

confidence: 99%

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Starvation‐induced autophagy promotes the invasion and migration of human bladder cancer cells via TGF‐β1/Smad3‐mediated epithelial‐mesenchymal transition activation

Tong

Yin

Hossain

et al. 2018

J of Cellular Biochemistry

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The biological characteristics of bladder cancer include enhanced invasion and migration, which are the main causes of death in patients. Starvation is a typical feature of the bladder cancer microenvironment and can induce autophagy. Autophagy has an important relationship with the invasion and migration of tumors. However, the role of autophagy in the invasion and migration of bladder cancer cells remains unclear. Hence, the aim of the current study was to clarify this role and underlying mechanism. In this study, we found that starvation enhanced the epithelial‐mesenchymal transition (EMT)‐mediated invasion and migration of T24 and 5637 cells while inducing autophagy. The inhibition of autophagy with chloroquine (CQ) or 3‐methyladenine (3MA) decreased EMT‐mediated invasion and migration. In addition, the expression of transforming growth factor 1 (TGF‐β1) and phosphorylated Smad3 (p‐Smad3) increased after starvation. The inhibition of autophagy with CQ or 3MA also decreased the expression of TGF‐β1 and p‐Smad3. The inhibitor of TGF‐β receptor sb431542 also inhibited the invasion, migration, and EMT of T24 and 5637 cells during starvation. Furthermore, recombinant TGF‐β1 induced autophagy and inhibition of the TGF‐β/Smad signaling pathway with sb431542 suppressed autophagy. In summary, our results suggested that autophagy promotes the invasion and migration of bladder cancer cells by inducing EMT through the TGF‐β1/Smad3 signaling pathway. Moreover, autophagy and TGF‐β1 can form a positive feedback loop to synergistically promote invasion and migration. Thus, our findings may provide a theoretical basis for the prevention of invasion and migration in bladder cancer.

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“…TGFβ1 enhances bovine fibroblast proliferation through the MAPK/Erk pathway (Gao et al, 2016), and promotes the transition of fibroblasts to myofibroblasts (De Vries et al, 2011); the latter are key mediators of ECM protein synthesis and tissue fibrosis (Phan, 2008). Furthermore, TGFβ1 is known to cause bovine mammary epithelial cells to switch to a mesenchymal phenotype through a process known as epithelial-to-mesenchymal transition (EMT) (Chen et al, 2017). In bovine mammary epithelial cells, EMT was reported to occur (at least in part) through the Smad pathway (Chen et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Peer Review #2 of "TGF-beta signalling in bovine mammary gland involution and a comparative assessment of MAC-T and BME-UV1 cells as in vitro models for its study (v0.2)"

Werling¹

2019

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The goal of the dairy industry is ultimately to increase lactation persistency, which is the length of time during which peak milk yield is sustained. Lactation persistency is determined by the balance of cell apoptosis and cell proliferation; when the balance is skewed toward the latter, this results in greater persistency. Thus, we can potentially increase milk production in dairy cows through manipulating apoptogenic and antiproliferative cellular signalling that occurs in the bovine mammary gland. Transforming growth factor beta 1 (TGFβ1) is an antiproliferative and apoptogenic cytokine that is upregulated during bovine mammary gland involution. Here we discuss possible applications of TGFβ1 signalling for the purposes of increasing lactation persistency. We also compare the features of MAC-T and BME-UV1 cells, two popular bovine mammary epithelial cell lines, to assess their appropriateness for the study of TGFβ1 signalling. TGFβ1 induces apoptosis and arrests cell growth in BME-UV1 cells, and this was reported to involve suppression of the somatotropic axis. Conversely, there is no proof that exogenous TGFβ1 induces apoptosis of MAC-T cells.In addition to TGFβ1's different effects on apoptosis,hormones and growth factors have distinct effects on TGFβ1 secretion and synthesis in MAC-T and BME-UV1 cell lines. MAC-T and BME-UV1 cells may behave differently in response to TGFβ1 due to their contrasting phenotypes; MAC-T cells have a profile indicative of both myoepithelial and luminal populations, while the BME-UV1 cells exclusively contain a luminal-like profile. Depending on the nature of the research question, the use of these cell lines as models to study TGFβ1 signalling should be carefully tailored to the questions asked.

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TGF-β1 Induces EMT in Bovine Mammary Epithelial Cells Through the TGFβ1/Smad Signaling Pathway

Cited by 57 publications

References 43 publications

A novel long non‐coding RNA regulates the immune response in MAC‐T cells and contributes to bovine mastitis

A novel long non‐coding RNA regulates the immune response in MAC‐T cells and contributes to bovine mastitis

Starvation‐induced autophagy promotes the invasion and migration of human bladder cancer cells via TGF‐β1/Smad3‐mediated epithelial‐mesenchymal transition activation

Peer Review #2 of "TGF-beta signalling in bovine mammary gland involution and a comparative assessment of MAC-T and BME-UV1 cells as in vitro models for its study (v0.2)"

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