Epithelial Cell Adhesion Molecule (EpCAM) Complex Proteins Promote Transcription Factor-mediated Pluripotency Reprogramming

Liao

Journal of Biological Chemistry

et al. 2012

113

Background: EpCAM is highly expressed on tumor and tumor-initiating cells. Results: EpCAM induces reprogramming factor and EMT gene expression, which regulates tumor self-renewal and tumorigenesis. Conclusion: EpCAM-mediated self-renewal and initiation of tumor cells are regulated by inducing reprogramming factors expressions. Significance: Our data reveal the mechanism underlying EpCAM-mediated tumor initiation and tumorigenesis of tumorinitiating cells in colon cancer.

Section: Discussionmentioning

confidence: 99%

“…Additionally, the expression of EpCAM is involved in the reprogramming process of induced pluripotent stem cells (14). Therefore, it is necessary to unveil the mechanism and functional roles of EpCAM and EpICD in TICs.…”

mentioning

confidence: 99%

Epithelial Cell Adhesion Molecule Regulates Tumor Initiation and Tumorigenesis via Activating Reprogramming Factors and Epithelial-Mesenchymal Transition Gene Expression in Colon Cancer

Liao

Journal of Biological Chemistry

et al. 2012

113

“…17, 18, 20, 21, 27, 58, 83, 93-98). Interestingly, recent studies showed that some of these liver CSC markers are also functionally involved in the maintenance of (99,100), and CD133 expression is required for the maintenance of CD133 + liver CSCs through neurotensin/ IL-8/CXCL1 signaling activation (101). In addition, a CD44 variant regulates the redox status by stabilizing xCT and protecting CSCs from oxidative stress (102), while CD13 reduces cell damage induced by oxidative stress after exposure to genotoxic reagents (19).…”

Section: Shared Features Of Liver Development and Liver Cancer Develomentioning

confidence: 99%

Cancer stem cells in the development of liver cancer

Yamashita

Wang²

2013

J. Clin. Invest.

465

431

Liver cancer is an aggressive disease with a poor outcome. Several hepatic stem/progenitor markers are useful for isolating a subset of liver cells with stem cell features, known as cancer stem cells (CSCs). These cells are responsible for tumor relapse, metastasis, and chemoresistance. Liver CSCs dictate a hierarchical organization that is shared in both organogenesis and tumorigenesis. An increased understanding of the molecular signaling events that regulate cellular hierarchy and stemness, and success in defining key CSC-specific genes, have opened up new avenues to accelerate the development of novel diagnostic and treatment strategies. This Review highlights recent advances in understanding the pathogenesis of liver CSCs and discusses unanswered questions about the concept of liver CSCs.

“…Interestingly, Zeb1 (a known transcription factor inducing EMT) represses both E-cadherin and EpCAM by binding to the EpCAM promoter [133], yet the expression of E-cadherin and EpCAM is related to a stem cell-like phenotype [134,135]; in basal-like breast cancer, EpCAM and P-cadherin both appear to be associated with the CSC phenotype [108]. As described for the hallmarks of cancer [33], the timing and ordering of these events appears to differ between normal and tumourous tissues, between different tissue and tumour types, and most likely within the same tumour.…”

Section: Cadherins and Epcammentioning

confidence: 99%

Cell adhesion and urothelial bladder cancer: the role of cadherin switching and related phenomena

Bryan

2015

Phil. Trans. R. Soc. B

Cadherins are mediators of cell-cell adhesion in epithelial tissues. E-cadherin is a known tumour suppressor and plays a central role in suppressing the invasive phenotype of cancer cells. However, the abnormal expression of N-and P-cadherin ('cadherin switching', CS) has been shown to promote a more invasive and m alignant phenotype of cancer, with P-cadherin possibly acting as a key mediator of invasion and metastasis in bladder cancer. Cadherins are also implicated in numerous signalling events related to embryonic development, tissue morphogenesis and homeostasis. It is these wide ranging effects and the serious implications of CS that make the cadherin cell adhesion molecules and their related pathways strong candidate targets for the inhibition of cancer progression, including bladder cancer. This review focuses on CS in the context of bladder cancer and in particular the switch to P-cadherin expression, and discusses other related molecules and phenomena, including EpCAM and the development of the cancer stem cell phenotype.