The basics of epithelial-mesenchymal transition

Kalluri, Raghu; Weinberg, Robert A.

doi:10.1172/jci39104

Cited by 8,243 publications

(6,426 citation statements)

References 132 publications

Supporting

Mentioning

6,285

Contrasting

Unclassified

Order By: Relevance

“…The developmental program of epithelial‐mesenchymal transition (EMT) has been confirmed to play a pivotal role in promoting metastasis in epithelium‐derived carcinoma 31, 32, 33, 34, 35. During the oncogenesis process, epithelial tumor cells underwent EMT and displayed an enhanced invasive and metastatic capacity 36, 37. In our study, the expression of E‐cadherin and vimentin (epithelial markers) were significantly increased in shDPP9‐transfected cells.…”

Section: Discussionmentioning

confidence: 53%

Contribution of upregulated dipeptidyl peptidase 9 (DPP9) in promoting tumoregenicity, metastasis and the prediction of poor prognosis in non‐small cell lung cancer (NSCLC)

Tang

Shen

et al. 2017

Intl Journal of Cancer

View full text Add to dashboard Cite

Dipeptidyl peptidase 9 (DPP9) is encoded by DPP9, which belongs to the DPP4 gene family. Proteins encoded by these genes have unique peptidase and extra‐enzymatic functions that have been linked to various diseases including cancers. Here, we describe the expression pattern and biological function of DPP9 in non‐small‐cell lung cancer (NSCLC). The repression of DPP9 expression by small interfering RNA inhibited cell proliferation, migration, and invasion. Moreover, we explored the role of DPP9 in regulating epithelial‐mesenchymal transition (EMT). The epithelial markers E‐cadherin and MUC1 were significantly increased, while mesenchymal markers vimentin and S100A4 were markedly decreased in DPP9 knockdown cells. The downregulation of DPP9 in the NSCLC cells induced the expression of apoptosis‐associated proteins both in vitro and in vivo. We investigated the protein expression levels of DPP9 by tissue microarray immunohistochemical assay (TMA‐IHC) (n = 217). Further we found mRNA expression levels of DPP9 in 30 pairs of clinical NSCLC tissues were significantly lower than in the adjacent non‐cancerous tissues. Survival analysis showed that the overexpression of DPP9 was a significant independent factor for poor 5‐year overall survival in patients with NSCLC (p = 0.003). Taken together, DPP9 expression correlates with poor overall survival in NSCLC.

show abstract

Section: Discussionmentioning

confidence: 53%

Contribution of upregulated dipeptidyl peptidase 9 (DPP9) in promoting tumoregenicity, metastasis and the prediction of poor prognosis in non‐small cell lung cancer (NSCLC)

Tang

Shen

et al. 2017

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…During tumor progression, the EMT has been generally accepted, which empowers the migratory and invasive abilities of tumor cells 3, 26. To further verify whether FLI‐1 can affect the invasiveness and metastasis of breast cancer cells, we performed wound‐healing and transwell assays after the knockdown of FLI‐1.…”

Section: Resultsmentioning

confidence: 99%

“…The EMT and CSC‐like properties are the malignant phenotypes of cancers,26, 38 the former contributes to invasion, migration, and metastasis; and the latter endows tumor cells with the capacity of tumorigenesis, recurrence, and therapy resistance 3, 27, 39, 40. All these factors are responsible for the poor prognosis of breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Friend leukemia virus integration 1 is a predictor of poor prognosis of breast cancer and promotes metastasis and cancer stem cell properties of breast cancer cells

et al. 2018

Cancer Medicine

View full text Add to dashboard Cite

Breast cancer is the most common cancer in women worldwide; despite the developments in diagnosis and therapy, recurrence and metastasis remain the main causes of death among patients with breast cancer. This study aimed to identify a promising biomarker for this disease. The study clarified (1) the association between Friend leukemia virus integration 1 (FLI‐1) and various molecular subtypes and (2) the prognostic value of FLI‐1 in breast cancer. To the best of our knowledge, this study is the first to report that FLI‐1 is a predictor of poor prognosis in patients with breast cancer and overexpressed in the triple negative breast cancer (TNBC) subtype. To further verify the effect of FLI‐1 in promoting the metastasis of TNBC, we performed a series of functional experiments in vitro and orthotopic xenograft experiments in the mammary fat pad of nude mice. FLI‐1, as a transcription factor, bound to the promoters of key EMT‐related genes (CDH1 and VIM), and regulated their expressions at the transcriptional level, thus induced epithelial‐mesenchymal transition (EMT). The overexpression of FLI‐1 significantly upregulated the expression of mesenchymal markers. After the modulation of FLI‐1, the changes in mammary stem cell markers (ALDH1A1 and CD133) and the capacity to form mammospheres were consistent with those of the EMT‐related markers. The orthotopic xenograft models further confirmed that the attenuation of stem cell traits after silencing FLI‐1 decreased the ability of tumorigenesis. These results indicate that FLI‐1 is a useful predictor of poor prognosis in patients with breast cancer. Furthermore, the preliminary exploration of metastatic mechanism in the patients with TNBC will provide a potential target to treat breast cancer in the near future.

show abstract

“…EMT is characterized by the loss of an epithelial phenotype, including expression of E‐cadherin, and the acquisition of mesenchymal markers such as fibronectin, vimentin, and N‐cadherin. Many distinct molecular processes occur during EMT including activation of transcription factors, expression of specific cell‐surface proteins, reorganization of cytoskeletal proteins, and production of extracellular matrix‐degrading enzymes 68. As a result, tumor cells develop increasing invasive and migratory potential.…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs in glioblastoma multiforme pathogenesis and therapeutics

Harish²,

et al. 2016

View full text Add to dashboard Cite

Glioblastoma multiforme (GBM) is the most common and lethal cancer of the adult brain, remaining incurable with a median survival time of only 15 months. In an effort to identify new targets for GBM diagnostics and therapeutics, recent studies have focused on molecular phenotyping of GBM subtypes. This has resulted in mounting interest in microRNAs (miRNAs) due to their regulatory capacities in both normal development and in pathological conditions such as cancer. miRNAs have a wide range of targets, allowing them to modulate many pathways critical to cancer progression, including proliferation, cell death, metastasis, angiogenesis, and drug resistance. This review explores our current understanding of miRNAs that are differentially modulated and pathologically involved in GBM as well as the current state of miRNA‐based therapeutics. As the role of miRNAs in GBM becomes more well understood and novel delivery methods are developed and optimized, miRNA‐based therapies could provide a critical step forward in cancer treatment.

show abstract

The basics of epithelial-mesenchymal transition

Cited by 8,243 publications

References 132 publications

Contribution of upregulated dipeptidyl peptidase 9 (DPP9) in promoting tumoregenicity, metastasis and the prediction of poor prognosis in non‐small cell lung cancer (NSCLC)

Contribution of upregulated dipeptidyl peptidase 9 (DPP9) in promoting tumoregenicity, metastasis and the prediction of poor prognosis in non‐small cell lung cancer (NSCLC)

Friend leukemia virus integration 1 is a predictor of poor prognosis of breast cancer and promotes metastasis and cancer stem cell properties of breast cancer cells

MicroRNAs in glioblastoma multiforme pathogenesis and therapeutics

Contact Info

Product

Resources

About