Molecular regulation of epithelial-to-mesenchymal transition in tumorigenesis (Review)

Škovierová, Henrieta; Okajčeková, Terézia; Strnádel, Ján; Vidomanová, Eva; Halašová, Erika

doi:10.3892/ijmm.2017.3320

Cited by 69 publications

(77 citation statements)

References 128 publications

(157 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Through EMT, epithelial cells lose epithelial phenotype-like cell polarity and connectivity to the basement membrane, but show a stronger ability of migration and invasion, similar to mesenchymal cells. 37 CCL2 derived from tumorassociated fibroblasts induced FGFR4 expression in colorectal cancer cells. 18 In contrast, tumor-associated fibroblasts could largely produce FGF19, which in turn activated FGFR4 in tumor cells.…”

Section: Aberrant Regulation Of Fgfr4 Ligandsmentioning

confidence: 95%

“…Epithelial‐mesenchymal transformation (EMT) plays an important role in embryonic development, chronic inflammation, tissue remodeling, various fibroid diseases and cancer metastasis. Through EMT, epithelial cells lose epithelial phenotype‐like cell polarity and connectivity to the basement membrane, but show a stronger ability of migration and invasion, similar to mesenchymal cells . CCL2 derived from tumor‐associated fibroblasts induced FGFR4 expression in colorectal cancer cells .…”

Section: Mechanisms Of Oncogenic Fgfr4 Signalingmentioning

confidence: 99%

See 1 more Smart Citation

Role of fibroblast growth factor receptor 4 in cancer

et al. 2018

View full text Add to dashboard Cite

Fibroblast growth factor receptors (FGFR) play a significant role in both embryonic development and in adults. Upon binding with ligands, FGFR signaling is activated and triggers various downstream signal cascades that are implicated in diverse biological processes. Aberrant regulations of FGFR signaling are detected in numerous cancers. Although FGFR4 was discovered later than other FGFR, information on the involvement of FGFR4 in cancers has significantly increased in recent years. In this review, the recent findings in FGFR4 structure, signaling transduction, physiological function, aberrant regulations, and effects in cancers as well as its potential applications as an anticancer therapeutic target are summarized.

show abstract

Section: Aberrant Regulation Of Fgfr4 Ligandsmentioning

confidence: 95%

Section: Mechanisms Of Oncogenic Fgfr4 Signalingmentioning

confidence: 99%

Role of fibroblast growth factor receptor 4 in cancer

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Cells adopt a spindle-shaped, mesenchymal-like morphology with upregulated expression of mesenchymal markers, such as N-cadherin, fibronectin and vimentin [45]. The molecular changes during EMT are well described in the current literature (reviewed: [46,47]). These changes are controlled by several signaling pathways (TGF-β1, Wnt, Notch, Hedgehog) and transcription factors (TWIST1, SNAIL1, SLUG, ZEB1 and/or FOXC1/2) [46,48].…”

Section: Epithelial-to-mesenchymal Transition (Emt)mentioning

confidence: 99%

Circulating Tumor Cells in Early and Advanced Breast Cancer; Biology and Prognostic Value

Fabisiewicz

Szostakowska-Rodzoś

Żaczek

et al. 2020

IJMS

View full text Add to dashboard Cite

Breast cancer metastasis is the leading cause of cancer deaths in women and is difficult to combat due to the long periods in which disseminated cells retain a potential to be re-activated and start the relapse. Assessing the number and molecular profile of circulating tumor cells (CTCs) in breast cancer patients, especially in early breast cancer, should help in identifying the possibility of relapse in time for therapeutic intervention to prevent or delay recurrence. While metastatic breast cancer is considered incurable, molecular analysis of CTCs still have a potential to define particular susceptibilities of the cells representing the current tumor burden, which may differ considerably from the cells of the primary tumor, and offer more tailored therapy to the patients. In this review we inspect the routes to metastasis and how they can be linked to specific features of CTCs, how CTC analysis may be used in therapy, and what is the current status of the research and efforts to include CTC analysis in clinical practice.There are two main hypotheses describing cancer dissemination: linear progression, according to which, metastatic potential is gained gradually, and the whole process proceeds in steps and needs time, and parallel progression, according to which dissemination takes place early on, even before clinical manifestation of the tumor [6,7] (Figure 1). In the linear progression model, the evolving primary tumor gives rise to metastases due to increasingly aggressive and invasive phenotypes of the subclones of tumor cells. This model is in agreement with the postulated role of the epithelial-to-mesenchymal transition (EMT) in cancer and assumes active degradation of the stroma and migration into blood vessels by the motile, invasive single cells that broke loose from the epithelial monolayer. In contrast to that, parallel progression postulates intravasation by passive shedding, which may take place shortly after the angiogenic switch, occurring during the early, pre-invasive stage of tumor development [8,9].

show abstract

“…38,40 A number of elements are important factors in regulation of gene expression and EMT, while referred to development of TNBC. [41][42][43][44] Moreover, the transcriptional regulation mechanism of EMT and how miRNA modulated EMT or development of TNBC was unclear yet. Recent research revealed that miR-34 might serve as inhibitor in nasopharyngeal carcinoma (NPC) by targeting Fig.…”

Section: Discussionmentioning

confidence: 99%

miR-425 suppresses EMT and the development of TNBC (triple-negative breast cancer) by targeting the TGF-β 1/SMAD 3 signaling pathway

Liu

Chen

2019

RSC Adv.

View full text Add to dashboard Cite

Background: EMT has a crucial effect on the progression and metastasis of tumors. This work will elucidate the role of miR-425 in EMT and the development of TNBC. Methods: The differential miRNA expression among non-tumor, para-tumor (adjacent tissue of tumor) and tumor tissues was analyzed. The luciferase activities of TGF-b1 3 0 UTR treated with miR-425 were determined. Then human breast cancer cell lines were treated with mimics or inhibitors of miR-425, and then the cell proliferation and migration, and invasion ability were assessed. The expression of TGF-b1 and markers of epithelial cells and mesenchymal cells were analyzed. The influences of miR-425 on the development of TNBC through inducing EMT by targeting the TGF-b1/SMAD3 signaling pathway in TNBC cell lines were investigated. Furthermore, xenograft mice were used to explore the potential roles of miR-425 on EMT and the development of TNBC in vivo. Results: Compared with non-tumor tissues, 9 miRNAs were upregulated and 3 miRNAs were down-regulated in tumor tissues. The relative expression of miR-425 in tumor tissues was obviously much lower than that in para-tumor and non-tumor tissues. MiR-425 suppressed TGF-b1 expression, and further inhibited expression of mesenchymal cell markers, while it exerted effects on cell proliferation and migration of TNBC cell lines. Moreover, the agomir of miR-425 could protect against the development process in a murine TNBC xenograft model. Conclusions: Our results demonstrated that miR-425 targets TGF-b1, and was a crucial suppressor on EMT and the development of TNBC through inhibiting the TGF-b1/SMAD3 signaling pathway. This suggests that aiming at the TGF-b1/SMAD3 signaling pathway by enhancing relative miR-425 expression, is a feasible therapy strategy for TNBC. RNA extractionTRIzol method was used to extract total RNA from tissues based on the operation manual. Then, smaller RNA (<200 nt) was removed with mirVana RNA isolation kit (Cat. no. AM27828; Invitrogen Thermo Fisher Scientic, Inc., Waltham, MA, USA) according to the instructions for manufacturer. Culture of cellThe cell lines of human TNBC, including MDA-MB-231 (ATCC® HTB-26™) and Hs 578T (ATCC® HTB-126™) were purchased from ATCC (American Type Culture Collection), and then cultured in DMEM with 10% FBS accompanied by Streptomycin and Penicillin (bi-antibiotics) with atmosphere (5% CO 2 ) at 37 C. siRNA for TGF-b1The well known siRNA of TGF-b1 supported by ref. 26 had been used in our study, which had been used as a positive in our study. The siRNA duplexes for TGF-b1 sequences are 5 0 -152 | RSC Adv., 2019,9,[151][152][153][154][155][156][157][158][159][160][161][162][163][164][165] This journal is Fig. 8 MiR-425 suppressed cell invasion of TNBC cell lines. Moreover, the inhibitors of miR-425 promoted invasion ability of TNBC cell lines, but the mimics of miR-425 suppressed the invasion ability of TNBC cell lines.This journal is Fig. 9 MiR-425 agomir suppressed TNBC xenografts. To detect anti-tumor activity induced by miR-425 agomir in vivo, human TNBC ...

show abstract

Molecular regulation of epithelial-to-mesenchymal transition in tumorigenesis (Review)

Cited by 69 publications

References 128 publications

Role of fibroblast growth factor receptor 4 in cancer

Role of fibroblast growth factor receptor 4 in cancer

Circulating Tumor Cells in Early and Advanced Breast Cancer; Biology and Prognostic Value

miR-425 suppresses EMT and the development of TNBC (triple-negative breast cancer) by targeting the TGF-β 1/SMAD 3 signaling pathway

Contact Info

Product

Resources

About