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Page 10 of 12 Park et al. J Cancer Metastasis Treat 2019;5:17 I http://dx.doi.org/10.20517/2394-4722.2018.84

A B

C

Figure 5. AF1q reciprocally regulates the expression of ICAM-1 in Burkitt’s lymphoma. A: ICAM-1 mRNA expression was quantified using
qPCR in MDA-MB-231LN cells engineered to overexpress or suppress AF1q; B: Western blot analysis of ICAM-1 and AF1q in Burkitt’s
lymphoma cell lines; C: representative images of AF1q and ICAM-1 staining in human Burkitt’s lymphoma tumor metastasis tissues. High
IHC staining of AF1q in tissue samples show low ICAM-1 expression

we reported that AF1q enhances the TCF7/LEF/β-catenin complex binding affinity as a cofactor. When we
performed immunoprecipitation with NF-κB antibody in cancer cells overexpressing AF1q, we observed that
β-catenin and AF1q were pulled down together (data not shown). However, it is not clear yet whether AF1q
promotes protein interaction between β-catenin and NF-κB. These results suggest that activated β-catenin by
AF1q would archive higher affinity to bind with NF-κB.

Cancer cells utilize multiple mechanisms to prevent host immune cells from exercising their antitumor
activities. Many of these mechanisms are now known on a cellular and molecular level. These mechanisms,
which enable the tumor to escape from the host immune system and to progress, are being intensively
investigated in hope of finding therapeutically safe and effective inhibitors able to counteract tumor-induced
immunosuppression. Tumor escape has been a major problem in cancer immunotherapy, and it has been
held responsible for the failure of many immune interventions in cancer. For this reason, it is important to
study and understand the various suppressive pathways human tumors utilize.

[21]
Tumors use blood vessels to supply themselves with oxygen and nutrients as well as for waste removal .
Lymphocytes also use blood vessels as the gateway where intergrin interactions with endothelial cell
adhesion molecules are required to infiltrate into the tumor [22,23] . The downregulation of ICAM-1 by several
inhibitory mechanisms limiting T cell transendothelial migration have been described [24-26] . Also, other
componets of the tumor stroma and cancer-associated fibroblasts, can suppress T cell infiltration, which can
[27]
influence cancer progression and metastasis .
The interction between tumor and lymphocytes through ICAM-1 plays an important role in leukocyte
adhesion, transduction, and cytolysis [28-30] . For example, tumor clones from melanoma metastasis split