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Abstract: The epithelial cell adhesion molecule is overexpressed in a variety of human cancers, including lung cancer, and its role in increased proliferation by up-regulating cell cycle accelerators, such as cyclin A/E, is well documented in breast and gastric cancers. In addition, the role of EpCAM in lung cancer pathogenesis remains to be investigated. Materias and methods: 18 human non-small cell lung cancer cell lung cancer cell lines and an immortalized human epithelial cell line were used. Three non-small cell lung cancer cell carcinoma cell and HBEC4 cells were used for EpCAM by RNA interference-mediated gene silencing. Results: We investigated EpCAM expression in a panel of lung cancer cell and HBEC4 lines and discovered that the majority of lung cancer cell lines expressed EpCAM. In anchorage dependent and non-dependent conditions, two EpCAM-expressing lung cancer cell lines with two EpCAM-expressing lung cancer cell lines demonstrated decreased proliferation and clonogenic growth, according to EpCAM's knockdown. EpCAM knockdown dampened invasion in a highly invasive segment but not in a lowly invasive cell line. In addition, EpCAM knockdown produced significant apoptosis in both cell lines and another EpCAM-expressing lung cancer cell line, but to a lesser extent in the HBEC4 line. In part, by up-regulating p27kip1 cyclin dependent kinase inhibitor, EpCAM knockdown caused lung cancer cells to be more responsive to contact inhibition. These findings show that EpCAM plays a major role in lung cancer development, particularly in its survival, and that the development of EpCAM-targeted therapy for lung cancer may have promise.
Source link: https://doi.org/10.1158/1538-7445.am2011-1657
Abstract Background: Breast cancer is the second leading cause of cancer-related deaths in American women. In the VERSA and subsequent mRNA extraction for the estrogen receptor and other breast cancer-relevant parameters, EpCAM positive CTCs were captured by EpCAM positive CTCs. The captured CTCs were tested for ER protein staining strength and localization. The VERSA platform was designed to capture and enumerate CTCs from breast cancer patients using EpCAM capture and immunofluorescent staining for intact nucleus, ER, and cytokeratin, although negative for multiple immune markers. In MCF7 and T47D cell lines, the VERSA can capture cells with > 90 percent capture rate with EpCAM antibody. A ER-specific transcriptome analysis of BC patient CTCs and cell lines was carried out, as well as cell lines. In 6 out of 7 BC samples, we found expression of ER in 6 out of 7 BC samples. Expression of PR and HER2 in a subset of samples indicates the collection of breast cancer cells for further molecular interrogation. Conclusion: We present the expression profiles of ER signaling genes in EpCAM captured CTCs from BC patients in conclusion. These tools will be used to analyze subpopulations of CTCs from patients with BC as predictive and pharmacodynamic biomarkers of response to regulated therapies or chemotherapies. In an epithelial cell adhesion molecule that captured circulating tumor cells from breast cancer patients with breast cancer patients with estrogen receptor specific signaling transcriptome [abstract]. The American Association for Cancer Research Annual Meeting, 2017-04-05; Washington, D. C. , 1-5; Proceedings of the American Association for Cancer Research Annual Meeting, 2017; 2017 Apr 1-5; 2017-04-05; Washington, D. C.
Source link: https://doi.org/10.1158/1538-7445.am2017-3784
Abstract Aims: Prostate cancer is the most common cancer in males in Australia, causing more than 3000 deaths in 2015 and is the most common cancer in males in Australia. EpCAM was highly expressed in metastatic CaP cell lines, primary human CaP tissues, and lymph node metastasis, according to our previous research, and is a biomarker involved in CaP formation, chemo-/radio-resistance. However, EpCAM's role in CaP growth and therapeutic resistance is still unclear. In vitro, Proliferation assay, colony formation assay, docetaxel, and radiation dose-response assay were carried out to investigate EpCAM's effect on proliferation and therapeutic response of CaP cells. To determine EpCAM's effect on CaP tumorigenecity, chemotherapy, and radiation response in NOD/SCID mice, subcutaneous and orthotopic CaP animal models were created using PC-3-EpCAM-KD and PC-3-EpCAM-scramble control cells in NOD/SCID mice. In three CaP cell lines, KD of EpCAM reduced CaP proliferative activity and improved DTX and radiation sensitivity, as well as increased sensitivity and enhanced radiation sensitivity. In NOD/SCID mice, both s. c and orthotopic EpCAM-KD xenografts showed reduced tumor formation and increased DTX and radiation responsiveness, as compared to EpCAM-scr control xenografts. According to the control group, EpCAM improved median survival of tumor-bearing mice by 21. 5 days in comparison to the placebo group, and KD of EpCAM resulted in tumor-bearing mice who received docetaxel by 11 days, and radiotherapy by 12 days compared to the control group. A novel treatment-resistant CaP can be combined with chemotherapy/radiotherapy, which may be a new modality for treatment-resistant CaP.
Source link: https://doi.org/10.1158/1538-7445.am2017-2833
Background: The epithelial cell adhesion molecule is present in most epithelia and is involved in cell adhesion, proliferation, differentiation, and migration that are typical for morphogenesis, including cell-cell adhesion, differentiation, and migration. In vitro, a role for EpCAM in pancreatic morphogenesis had been reported. In addition, EpCAM expression patterns in embryonic lung and thymus, as well as in the regenerating liver were found in the regenerating liver. Methods: The expression pattern of human and murine homologues of EpCAM was found in adult and embryonic kidneys from humans and human-EpCAM -transgenic mice, according to immunohistochemistry. Results: EpCAM expression was found in the urine bud during nephrogenesis and nephrogenesis, according to EpCAM. Both epithelia and segment-specific nephron markers were found in adult kidneys, with varying amounts of EpCAM as revealed by double staining for human EpCAM and segment-specific nephron markers. In adult kidneys, the EpCAM protein transformed from apical in embryonic to basolateral. Conclusions: During nephrogenesis, EpCAM's spatiotemporal expression pattern changed.
Source link: https://doi.org/10.1159/000111039
Modulation of LCu2013keratinocyte adhesion is likely to be vital to regulation of LC migration. High LC antibodies are found to contain high amounts of epithelial cell adhesion molecule, a cell-surface protein that is characteristic of certain epithelia and some carcinomas, and has been implicated in intercellular adhesion and metastasis. In vitro, epidermis from these mice had elevated numbers of LC with normal amounts of MHC, costimulation proteins, and T-cell-u2013stimulatory function. Migration of EpCAM-deficient LC from skin explants was stopped, but chemotaxis of dissociated LC was not. As previously described in LC-deficient mice, Attenuated migration of EpCAM-deficient LC resulted in improved contact hypersensitivity responses. These results provide conclusively link EpCAM expression to LC motility/migration, and LC migration to immune regulation. EpCAM appears to promote epidermis migration by lowering LC/u2013keratinocyte adhesion, and may help to modulate intercellular adhesion and cell migration within epithelia during growth and carcinogenesis in an analogous manner.
Source link: https://doi.org/10.1073/pnas.1117674109
We investigated whether TAA, IL-2, IL-6, IL-12, interferon-alpha, and tumor necrosis factor-alpha can influence EpCAM and LewisY expression on the surface of the colorectal carcinoma cell lines HT29, Lovo, and SW480 cells. Since an elevated level of TAA can lead to increased antibody-dependent cellular cytotoxicity, we investigated whether the cytokines IL-2, IL-4, cytotoxic Only IFN-u03b1 increased strongly, but IL-4 slowed both EpCAM and LewisY expressions, according to we found. MoAb BR55-2 down-regulated LewisY antigen expression, but MoAb 17-1A, which binds to EpCAM, up-regulated this TAA after three days of culture. We found that 5-fluorouracil, mitomycin-C, and oxaliplatin up-regulated EpCAM and Lewisy antigen expression in subsequent experiments with chemotherapeutic drugs commonly used for the treatment of colorectal cancer. The combination of IFN-u03b1, 5-fluorouracil, and MoAb 17-1A produced the highest expression for EpCAM on HT29 cells.
Source link: https://doi.org/10.1046/j.1365-2249.2001.01435.x
Abstract EpCAM was first identified four decades ago as a tumor antigen on colorectal carcinomas. EpCAM, a diagnostic marker and a therapeutic target, as well as a key source of metastatic cancer cells, due to its widespread and high prevalence on carcinomas and metastases. EpCAM is recognized as a multi-functional transmembrane protein involved in cell adhesion, proliferation, stemness, and epithelial-to-mesenchymal transition of carcinoma cells. Both the WNT and Ras/Raf pathways's cellular signaling pathways interact with claudins, CD44, E-cadherin, epidermal growth factor receptor, and intracellular signaling components of the WNT and Ras/Raf pathways. EpCAM is a marker for primary and systemic tumor cells' epithelial status, and it appears as a measure of CTC metastatic capacity. EpCAM has reclaimed recognition as a diagnostic marker and target on primary and systemic tumor cells, according to Consequentially.
Source link: https://doi.org/10.1007/s10555-020-09898-3
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