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CDCP1 was the most significant (FDR adjusted p-value 0.006). Correlation with CDCP1 concentration was most significant for CD34+ concentration and nucleated cell count. Multivariate analysis showed that CD34 and gender seemed to influence the level of CDCP1.
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Study discovered a new mechanism of regulation of CDK5 through loss of CDCP1, which dynamically regulates beta1-integrin in non-adherent cells and which may promote vascular dissemination in patients with advanced prostate cancer.
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Study identified PDGF-BB/PDGFRbeta-mediated pathway as a novel player in the regulation of CDCP1 in triple-negative breast cancer through ERK1/2 activation.
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Low CDCP1 expression is associated with idiopathic pulmonary fibrosis.
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Expression of CDCP1 was reduced by AHCC treatment of KLM1-R cells, whereas expression of actin was not affected. The ratio of intensities of CDCP1/actin in AHCC-treated KLM1-R cells was significantly suppressed (p<0.05) compared to untreated cells.
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Co-expression of CDCP1 and AXL is often observed in EGFR-mutation-positive tumors, limiting the efficacy of EGFR TKIs. Co-treatment with EGFR TKI and TPX-0005 warrants testing.
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CDCP1 knockdown reduced 3D invasion, which can be rescued by ACSL3 co-knockdown. In vivo, inhibiting CDCP1 activity with an engineered blocking fragment (extracellular portion of cleaved CDCP1) lead to increased LD abundance in primary tumors, decreased metastasis, and increased ACSL activity in two animal models of TNBC.
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These results revealed that ADAM9 down-regulates miR-1 via activating EGFR signaling pathways, which in turn enhances CDCP1 expression to promote lung cancer progression.
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CDCP1 is a novel marker of the most aggressive N-positive triple-negative breast cancers; CDCP1 expression and gains in CDCP1 copy number synergized with nodal (N) status in determining disease-free and distant disease-free survival
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High expression level of CDCP1 is associated with recurrence in glioblastoma.
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These studies have important implications for the development of a therapeutic to block CDCP1 activity and Triple-negative breast cancer (TNBC)metastasis.
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CDCP1 may facilitate loss of adhesion by promoting activation of EGFR and Src at sites of cell-cell and cell-substratum contact.
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Stromal expression patterns for both ADAM12 and CDCP1.
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these data demonstrated that HIF-2alpha could promote hepatocellular carcinoma cell migration by regulating CDCP1
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Our results establish that differential glycosylation, cell surface presentation and extracellular expression of CDCP1 are hallmarks of prostate cancer progression.
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High CDCP1 expression is associated with Colorectal Cancer.
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ADAM9 enhances CDCP1 protein expression by suppressing miR-218 for lung tumor metastasis
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Elevated CDCP1 was observed in 77% of HGSC cases. Silencing of CDCP1 reduced migration and non-adherent cell growth in vitro and tumour burden in vivo.
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CDCP1 protein plays an important role in the progression of ovarian clear cell carcinoma. Elevated CDCP1 levels correlates with poor patient outcome in ovarian clear cell carcinoma patients.
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CDCP1 overexpression enhances HER2 activity. CDCP1 binds to HER2, promoting SRC-HER2 crosstalk.
