A genome-wide expression analysis identifies a network of EpCAM-induced cell cycle regulators

Maaser, Kerstin; Borlak, Jürgen

doi:10.1038/sj.bjc.6604725

Cited by 54 publications

(45 citation statements)

References 43 publications

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“…EPCAM expression has been found to be associated with cellular differentiation. Findings show that the germinal regions in normal colonic crypts display increased EPCAM expression but as the cells differentiate and migrate to the top of the villi, its expression decreases [38]. The reason for the reduction in the EPCAM expression might be due to the reduction of adhesion between the tendon and surrounding tissues after thermal preconditioning.…”

Section: Discussionmentioning

confidence: 99%

Thermal Preconditioning May Prevent Tendon Adhesion by Up-Regulating HSP72 in Rats

Tan

et al. 2017

Cell Physiol Biochem

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Background/Aims: The study aims to determine the effects of thermal preconditioning on tendon adhesion by regulating the expression of heat shock protein 72 (HSP72) in rat models. Methods: Sixty male Wistar rats were collected and randomly assigned into the thermal preconditioning and control groups. During the 4^th and 8^th weeks following surgery, 15 rats were sacrificed in each period respectively, and their tendon adhesion was observed and evaluated. Biomechanical testing was performed to measure the tensile strength and gliding distance of tendons. Hematoxylin-eosin (HE) was used to observe the morphological structure of the tendons. Immunohistochemical staining, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to detect the HSP72, fibroblast growth factor-2 (FGF-2), fibroblast growth factor receptor-1 (FGFR-1), β-catenin, epithelial cell adhesion molecule (EPCAM), Tenomodulin and scleraxis protein expressions. Pearson correlation analysis was applied to analyze the correlation between HSP72 expression and tendon adhesion. Results: At the 4^th week after surgery, we found no differences in the tendon adhesion scores or mRNA and protein expressions of HSP72 between the thermal preconditioning and control groups. However, after the 8^th week after surgery, the thermal preconditioning group had a lower tendon adhesion score and higher mRNA and protein expressions of HSP72 than the control group. During the same period, we found longer gliding distance and higher expression levels of FGF-2, FGFR-1, β-catenin, Tenomodulin and scleraxis, but lower EPCAM expression in the thermal preconditioning group. Pearson correlation analysis indicated that HSP72 mRNA and protein expression levels were negatively correlated with tendon adhesion. Conclusions: These findings provide evidence that thermal preconditioning may alleviate tendon adhesions via upregulation of HSP72 expression.

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Section: Discussionmentioning

confidence: 99%

Thermal Preconditioning May Prevent Tendon Adhesion by Up-Regulating HSP72 in Rats

Tan

et al. 2017

Cell Physiol Biochem

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“…The origin of NETs is still debated, but the expression of this carcinoma-associated antigen adds evidence to an epithelial origin rather than being derived from the neural crest as was once originally thought (10,19). EpCAM upregulates c-myc and cyclins, promoting cell cycling and enhancing proliferation (20)(21)(22)(23)(24). Anti-EpCAM therapy has been trialed in metastatic breast cancer, colorectal cancer, and in malignant ascites (25)(26)(27)(28)(29)(30) and EpCAM expression in NETs presents an opportunity for EpCAM directed therapy (9).…”

Section: Discussionmentioning

confidence: 99%

Circulating Tumor Cells and EpCAM Expression in Neuroendocrine Tumors

Khan

Tsigani

Rashid

et al. 2011

Clinical Cancer Research

104

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Purpose: Neuroendocrine tumors (NET) are heterogeneous tumors with widely variable survival. It is unknown whether they express EpCAM (epithelial cell adhesion molecule) and thus whether NET circulating tumor cells (CTC) are detectable. We systematically investigated EpCAM expression and CTC detection in patients with metastatic NETs and evaluated the potential of CTCs to predict radiological progression.Experimental Design: EpCAM protein expression was evaluated in 74 samples of formalin-fixed, paraffin-embedded NET tissue by immunohistochemistry. Seventy-nine patients with metastatic NETs (42 midgut, 5 unknown primary, 19 pancreatic, 13 bronchopulmonary) had blood samples drawn for CTC isolation and enumeration utilizing the CellSearch platform. Patients were classified as having progressive or nonprogressive disease on the basis of serial imaging.Results: Strong homogeneous, membranous EpCAM expression was observed in all ileal (n ¼ 26) and pancreatic NETs (n ¼ 16), whereas variable EpCAM expression was observed in bronchopulmonary NETs (n ¼ 13). Forty-three percent of midgut and 21% of pancreatic NETs had CTCs detected with a range of 0-62 and 0-11, respectively. The absence of CTCs was strongly associated with stable disease (P < 0.001). There was a moderate correlation between CTC levels and urinary 5-hydroxyindole acetic acid (r ¼ 0.5, P ¼ 0.007) and between CTC levels and burden of liver metastases (B ¼ 8.91, P < 0.001). There was no or low correlation between CTC levels and Ki-67 (r ¼ 0.08, P ¼ 0.59) and serum chromogranin A (r ¼ 0.246, P ¼ 0.03).Conclusions: This is the first systematic analysis showing EpCAM expression and CTC detection in NETs. CTCs seem to be associated with progressive disease and may provide useful prognostic information given the variable survival rates in these tumors.

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“…Expression of EpICD was capable of counteracting these deficiencies, and could alone enhance c-myc transcription and cell proliferation. A number of EpCAM-regulated target genes have been identified including c-myc and cyclins (7), and additional genes involved in cell growth and proliferation, cell cycle, and cell death (14).…”

Section: Epcam's Nuclear Signaling Complexmentioning

confidence: 99%

The Emerging Role of EpCAM in Cancer and Stem Cell Signaling

Münz¹,

Baeuerle²,

2009

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Initially discovered as a dominant antigen on colon carcinomas, the epithelial cell adhesion molecule (EpCAM) was considered a mere cell adhesion molecule and reliable surface-binding site for therapeutic antibodies. Recent findings can better explain the relevance of EpCAM's high-level expression on human cancers and cancer propagating cells, and its negative prognostic potential for survival of patients with certain cancers. EpCAM has oncogenic potential and is activated by release of its intracellular domain, which can signal into the cell nucleus by engagement of elements of the wnt pathway.

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A genome-wide expression analysis identifies a network of EpCAM-induced cell cycle regulators

Cited by 54 publications

References 43 publications

Thermal Preconditioning May Prevent Tendon Adhesion by Up-Regulating HSP72 in Rats

Thermal Preconditioning May Prevent Tendon Adhesion by Up-Regulating HSP72 in Rats

Circulating Tumor Cells and EpCAM Expression in Neuroendocrine Tumors

The Emerging Role of EpCAM in Cancer and Stem Cell Signaling

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