A meta-analysis and The Cancer Genome Atlas data of prostate cancer risk and prognosis using epithelial cell adhesion molecule (EpCAM) expression

Abstract

Background: Epithelial cell adhesion molecule (EpCAM) expression has been reported in many types of cancer, including prostate cancer (PCa). However, the role of EpCAM expression remains inconsistent. We conducted a meta-analysis to assess the clinicopathological and prognostic significance of EpCAM expression in PCa. Methods: Publications were searched online using electronic databases. The available data were obtained from The Cancer Genome Atlas (TCGA). The odds ratios (ORs) or hazard ratios (HRs) with their 95% confidence intervals (CIs) were calculated. Results: We identified seven studies in which immunohistochemistry was used and that included 871 prostatic tissue samples. EpCAM expression was significantly higher in PCa samples than in benign and normal tissue samples (OR = 77.93, P = 0.002; OR = 161.61, P < 0.001; respectively). No correlation of EpCAM overexpression with pT stage and lymph node metastasis was observed; however, EpCAM overexpression showed a significant correlation with Gleason score (OR = 0.48, P = 0.012) and bone metastasis (OR = 145.80, P < 0.001). Furthermore, TCGA data showed that EpCAM overexpression was not closely correlated with age, pT stage, lymph node metastasis, number of lymph node, prostate-specific antigen level, Gleason score, biochemical recurrence, and overall survival. Based on multivariate Cox proportional-hazards regression analysis, a significant correlation was observed between EpCAM overexpression and 5-year worse biochemical recurrence free-survival. Conclusions: EpCAM overexpression may be correlated with the development of bone metastasis and worse biochemical recurrence free-survival of PCa. Further studies are needed to verify these findings.

Influence of the Position and Composition of Radiometals and Radioiodine Labels on Imaging of Epcam Expression in Prostate Cancer Model Using the DARPin Ec1

“…Induction of EpCAM expression occurs early in prostate carcinogenesis and the expression increases with Gleason score and tumor stage [ 6 ]. EpCAM overexpression in PCa is associated with metastasis, resistance to chemo- and radiotherapy [ 8 , 9 ] and an increased risk of cancer recurrence [ 7 , 10 ], which makes it a promising therapeutic target.…”

Protein signatures to distinguish aggressive from indolent prostate cancer

“…The overexpression of these proteins in osteoblastic prostate cancer has been reported to be related to an increase in tumorigenicity in vivo 59 . Additional proteins of interest that were observed with significant increased levels in recurrent versus nonrecurrent patients in our data set include POSTN a secreted protein that has been associated with prostate cancer development and progression, 60 EPCAM a protein with expression levels correlated with Gleason score and bone metastasis in prostate cancer patients, 61 and RPSA a protein significantly associated with invasion and metastasis in pancreatic cancer 62 . Protein‐binding activity modulator (PC00095) and protein‐modifying enzymes (PC00260) such a DPP4, a protein that has been identified as a tumor suppressor gene during progression to castration‐resistant prostate cancer, 63 was observed to have decreased levels in recurrent prostate cancer.…”

The Predictive Role of Serum Levels of Soluble Cell Adhesion Molecules (sCAMs) in the Therapy of Advanced Breast Cancer—A Single-Centre Study

“…Most of the studies were devoted to the expression of EpCAM in tissues of epithelial-derived neoplasms [39][40][41]. Survival was estimated to be worse in patients with higher expression EpCAM in breast cancer tissue [39], especially in the luminal B HER2 positive and basal-like breast cancer [42,43], and ovarian [44], prostate [45], and gall bladder cancers [46]. In physiological conditions, this molecule plays a role in homotypic cell adhesion and is also involved in the cell differentiation and cell cycle by its capacity to upregulate cyclins A and E [47].…”