We evaluated epithelial-mesenchymal phenotypic characteristics across a range of tumor histologies using a validated, high resolution digital microscopic immunofluorescence assay (IFA) that incorporates β-catenin detection and cellular morphology to delineate carcinoma cells from stromal fibroblasts and that quantitates the individual and co-localized expression of the epithelial marker E-cadherin (E) and the mesenchymal marker vimentin (V) at subcellular resolution ("EMT IFA").
Vimentin represents the major protein associated with epithelial-mesenchymal transition (EMT), an essential process when the primary tumour transforms into a malignant one. mRNA and proteomic data obtained in this study, based on the PDQuest software protein evaluation and further quantification of proteins by iTRAQ analysis, suggest that vimentin was significantly reduced in the combination of RAR ligand and RXR ligand treatment.
The native tropism of CPMV for cell-surface displayed vimentin and the enhanced permeability and retention effect allow them to preferentially extravasate from tumor neovasculature and efficiently penetrate tumors.
Both tumor types were positive for TFE3 and vimentin; however, TFE3-M tumor cells expressed epithelial membrane antigen and human melanoma black-45 but not cluster of differentiation 10 (CD10), whereas the TFE3-N cells expressed P504S, CD10, and vimentin but not cytokeratin 7.
The carcinomatous and sarcomatous areas were immunoreactive for pan-cytokeratin and vimentin, respectively, while immunoreactivity for e-cadherin was restricted to the carcinomatous component of the neoplasm.
NSCLC tumor specimens exhibited higher circP4HB levels in comparison to paired healthy lung samples and was associated with metastatic disease and poorer survival. circP4HB promoted EMT and vimentin expression in vitro and xenograft metastasis in vivo through sequestration of miR-133a-5p.
Furthermore, hypermethylation of SOX1 and VIM promoters were found in patients with advanced TNM stage (III-IV) and larger tumor size (≥5 cm) compared with early stage (I-II) (p<0.001 and p=0.004) patients with smaller tumor size (<3 cm) (p=0.018 and p=0.001).
Moreover, the up-regulation of miR-539 or DLX1 gene silencing led to the inhibition of PCa cell proliferation, migration, invasion, EMT and tumour growth, accompanied by increased E-cadherin expression and decreased expression of vimentin, Smad4, c-Myc, Snail1 and SLUG.
By contrast, DEX inhibited miR‑132 expression via promoter methylation. miR‑132 mimics also reduced DEX‑induced clonogenicity, migration and expression of vimentin and E‑cadherin in vitro and in tumor xenografts.
It was found that molecules related to mesenchymal cells (vimentin and transglin), in addition to those related to tumor aggressiveness with potential secretory behavior (e.g. cathepsin B) were among differentially expressed proteins.
Immunohistochemical examination revealed that the number of tumour buds increased in patients with tumours showing a mesenchymal profile (negative for E-cadherin and positive for vimentin).
The expression of vimentin in the ESCC cells was significantly upregulated, the expression of E-cadherin was significantly downregulated, and the invasion and migration of the ESCC cells were significantly enhanced after tumour-associated macrophages were added to the co-culture.
By immunohistochemistry, the tumor cells were positive for vimentin and glial fibrillary acid protein, whereas negative for epithelial membrane antigen.
E-cadherin and N-cadherin were down-regulated in all tumor and normal cell lines studied, whereas vimentin expression increased in only two tumor and one normal cell line.
We analyzed datasets from The Cancer Genome Atlas to identify an immune profile associated with prolonged overall survival in multiple tumor types and tested the efficacy of tumor cell-surface vimentin-targeted interleukin 12 (ttIL-12) in inducing that immune profile and prolonging survival in both mouse and patient-derived xenograft tumor models.
HMGA2 expression, loss of E-cadherin and Vimentin expression were significantly associated with clinical stage, tumor differentiation and lymph node metastasis.
In vivo, injection of R9-ZnC<sup>S334D</sup> in 4T1 tumors impaired tumor growth, decreased tumor hypoxia, and expression of the epithelial-to-mesenchymal transition (EMT) markers Snail, Vimentin, and N-cadherin.
The expression of pSTAT3, phosphorylated extracellular signal-regulated kinase (pERK), PI3K, pAkt, snail, vimentin, and N-cadherin was significantly lower in tumors from IL-6 shRNA-treated MDA-MB cells.
There was no correlation between the percentage of cells expressing vimentin and α-SMA in the tumor stroma (Pearson's correlation coefficient: r = 0.171).
In addition, the status of PTEN, ABCC1/MRP1, ABCB1/MDR1, Bcl2, and vimentin in surgical specimens was also significantly associated with adverse clinicopathological factors in surgery specimens, suggesting that these alterations could be responsible for tumor relapse in TNBC patients.
The expression of VIM were lower (P<0.001) and that of E-cad was higher (P<0.001) in tumor tissue when compared with the normal tissue at the transcriptional level.