<i>Cinnamomum cassia</i>
 extracts reverses TGF-β1-induced epithelial-mesenchymal transition in human lung adenocarcinoma cells and suppresses tumor growth in vivo

Chen, Lin; Hsieh, Yi‐Hsien; Yang, Shun‐Fa; Chu, Shu‐Chen; Chen, Pei‐Ni; Hsieh, Yih‐Shou

doi:10.1002/tox.22410

Cited by 26 publications

(25 citation statements)

References 23 publications

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“…But there are other evidences that EpCAM might play a role in EMT and other pathophysiological aspects of migration and invasion. TGF‐β1 is usually regarded as an important inducer of EMT in different malignant tumors 40–45 . TGF‐β1 can lead to the EMT in MCF‐7 cells, as well as increased EpCAM.…”

Section: Discussionmentioning

confidence: 99%

Increased expression of epithelial cell adhesion molecule and its possible role in epithelial–mesenchymal transition in endometriosis

Liu

Yang

Liang

et al. 2020

J of Obstet and Gynaecol

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Aim: To study the involvement and interrelationship of epithelial cell adhesion molecule (EpCAM) and epithelial-mesenchymal transition (EMT) in endometriosis. Methods: Samples from 114 patients undergoing endometrial biopsy or operation for endometriosis and 23 premenopausal women undergoing endometrial biopsy for non-endometriotic benign disease. Immunohistochemistry was used to detect expression level of EpCAM, E-cadherin and N-cadherin in endometrium from patients with (n = 24) and without endometriosis (n = 23), and in lesions from bowel (n = 46), peritoneal (n = 20) and ovarian (n = 24) endometriosis. Results: There was no significant difference in the expression level of EpCAM, E-cadherin and N-cadherin, respectively, between endometrium from women with and without endometriosis (P > 0.05). There was also no significant difference in the expression level of EpCAM, E-cadherin and N-cadherin, respectively, among lesions from the bowel, peritoneal and ovarian endometriosis (P > 0.05). We found that the immunoreactivity of endometriotic epithelial cells to EpCAM and N-cadherin was significantly higher than that of eutopic endometrium, but decreased to E-cadherin (P < 0.05). According to the expression level of EpCAM, the expression level of E-Cadherin was significantly lower in endometriotic lesions with EpCAM expression above the mean level compared with that of endometriotic lesions with EpCAM expression below mean level, while the expression level of N-cadherin was contrary (P < 0.001). EpCAM staining level was negatively correlated with E-cadherin but positively correlated with N-cadherin (P < 0.001). Conclusions: These data suggest that overexpression of EpCAM, accompanied by an EMT, might be involved in endometriosis. EMT may be induced by the overexpression of EpCAM, thus promoting the development of endometriosis, which needs future studies to confirm for the pathogenesis of endometriosis.

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Section: Discussionmentioning

confidence: 99%

Increased expression of epithelial cell adhesion molecule and its possible role in epithelial–mesenchymal transition in endometriosis

Liu

Yang

Liang

et al. 2020

J of Obstet and Gynaecol

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“…Triplicate samples were tested, and data are expressed as the average cell number in five fields. The motility assay was conducted following similar instructions for the invasion assay except for the absence of Matrigel coating …”

Section: Methodsmentioning

confidence: 99%

Antimetastatic potentials of salvianolic acid A on oral squamous cell carcinoma by targeting MMP‐2 and the c‐Raf/MEK/ERK pathway

Fang

Chen

et al. 2018

Environmental Toxicology

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The metastasis of oral squamous cell carcinoma (OSCC) is one of the most important causes of cancer-related deaths. Thus, various therapeutic strategies have been developed to prevent the metastasis of OSCC. Salvianolic acid A (SAA), a traditional Chinese medicine, has antithrombosis, antiplatelet, anti-inflammation, and antitumor activities. Here, we provide molecular evidence indicating that SAA exerts its antimetastatic effects by markedly inhibiting the invasion and migration of oral squamous SCC-9 and SCC-25 cells. SCC-9 and SCC-25 cells were treated with various concentrations of SAA to further investigate the precise involvement of SAA in cancer metastasis. The results of zymography, and Western blotting indicated that SAA treatment may decrease matrix metallopoteinase-2 (MMP-2) expression. SAA also inhibited p-c-Raf, p-MEK1/2, and p-ERK1/2 protein expression. In addition, treating SCC-9 cells with U0126, a MEK-specific inhibitor, decreased MMP-2 expression and concomitantly inhibited cell migration. Our findings suggested that SAA inhibits the invasion and migration of OSCC by inhibiting the c-Raf/MEK/ERK pathways that control MMP-2 expression. Our findings provide new insights into the molecular mechanisms that underlie the antimetastatic effect of SAA and are thus valuable for the development of treatment strategies for metastatic OSCC.

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“…Cell migration and invasion assays were performed using 24‐well modified Boyden chambers containing membrane filter inserts with 8‐μm pores (Corning Incorporated Life Sciences, Tewksbury, MA) . Membrane filter inserts were pre‐coated with Matrigel Matrix (Corning Incorporated Life Sciences, Tewksbury, MA) for the invasion assays.…”

Section: Methodsmentioning

confidence: 99%

β‐mangostin suppresses human hepatocellular carcinoma cell invasion through inhibition of MMP‐2 and MMP‐9 expression and activating the ERK and JNK pathways

Huang

Teng

et al. 2017

Environmental Toxicology

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β-mangostin is a dietary xanthone that has been reported to have the anticancer properties in some human cancer cell types. However, the antimetastatic effect and molecular mechanism of β-mangostin action in human hepatocellular carcinoma (HCC) cells remain unknown. In this study, we found that β-mangostin did not induce cytotoxicity in human HCC cells (SK-Hep-1, Huh-7 and HA22T/VGH cells). β-mangostin could inhibit migration and invasion of human HCC cells. Meanwhile, β-mangostin significantly decreased the protein activities and expression of matrix metalloproteinase (MMP)-2 and MMP-9 via increasing the activation of MEK1/2, ERK1/2, MEK4 and JNK1/2 signaling pathways. Furthermore, using specific inhibitor for ERK1/2 (PD98059) and JNK1/2 (JNKII) significantly restored the expression of MMP-2/-9 and invasion by β-mangostin treatment in Huh-7 cells. In addition, β-mangostin effectively restored the protein levels and transcription activity of MMP-2 and MMP-9 in siERK or siJNK-transfected Huh-7 cells, concomitantly with promotion on cell migration and invasion. Taken together, these findings are the first to demonstrate the antimetastatic activity of β-mangostin against human HCC cells, which may act as a promising therapeutic agent for the treatment of HCC.

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Cinnamomum cassia extracts reverses TGF-β1-induced epithelial-mesenchymal transition in human lung adenocarcinoma cells and suppresses tumor growth in vivo

Cited by 26 publications

References 23 publications

Increased expression of epithelial cell adhesion molecule and its possible role in epithelial–mesenchymal transition in endometriosis

Increased expression of epithelial cell adhesion molecule and its possible role in epithelial–mesenchymal transition in endometriosis

Antimetastatic potentials of salvianolic acid A on oral squamous cell carcinoma by targeting MMP‐2 and the c‐Raf/MEK/ERK pathway

β‐mangostin suppresses human hepatocellular carcinoma cell invasion through inhibition of MMP‐2 and MMP‐9 expression and activating the ERK and JNK pathways

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