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Abstract
Tumor initiating cells (TICs) differ from normal stem cells (SCs) in their ability to initiate tumorigenesis, invasive growth, metastasis and the acquisition of chemo and/or radio-resistance. Over the past years, several studies have indicated the potential role of the Notch system as a key regulator of cellular stemness and tumor development. Furthermore, the expression of cancer testis antigens (CTA) in TICs, and their role in SC differentiation and biology, has become an important area of investigation. Here, we propose a model in which CTA expression and Notch signaling interacts to maintain the sustainability of self-replicating tumor populations, ultimately leading to the development of metastasis, drug resistance and cancer progression. We hypothesize that Notch–CTA interactions in TICs offer a novel opportunity for meaningful therapeutic interventions in cancer.
ACKNOWLEDGMENT
This work was supported by the Associate Dean for Oncology Programs at TTUHSC, The Billy and Ruby Power Endowment for Cancer Research, The Laura W. Bush Institute for Women's Health, Kiromic, LLC and Endowed Chair for Excellence in Women's Health Director of Breast Health Service.
Declaration of Interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the article.