Kamran Khan

Endostatin Regulation of MHC1 as a Mechanism of Immune Evasion in Circulating Tumor Cells

Kamran Khan^1,2 and Olorunseun Ogunwobi^1,2
1Department of Biological Sciences, Hunter College, City University of New York, New York, NY; ²Hunter College Center for Cancer Health Disparities Research (CCHDR), New York, NY

Metastasis is the leading cause of cancer deaths (1). Metastasis involves dissociation of cells from the primary tumor, circulation of these cells in the blood, and the formation of secondary tumors (1). These cells which have separated from the primary tumor and are traveling in the blood are circulating tumor cells (CTCs) (1, 2). These CTCs are a critical step in metastasis. Several molecular changes have to take place for these primary tumor cells to dissociate and circulate in the bloodstream (1). One characteristic of these CTC’s is that they are able to circulate in the bloodstream while successfully evading being destruction by the immune system (3). We have previously demonstrated that CTCs have significantly lower cell surface expression of an important cell surface protein called major histocompatibility complex class 1 (MHC1) is less expressed in CTCs as compared to primary tumor cells and it also shows a cytokine called endostatin that is less secreted in CTCs as compared to primary tumor cells (1). The under-expression of MHC1 in CTCs may allow CTCs to evade the immune system. In this study we are hypothesizing that decreased endostatin secretion in CTCs is what causes lower MHC1 cell surface expression via IFN-y signaling and serves as a mechanism of immune evasion for CTCs.

Email questions and comments about this abstract to KAMRAN.KHAN86@myhunter.cuny.edu.