ICAM-1, as a surface glycoprotein, is expressed on vascular endothelium, macrophages, and activated lymphocytes, and mediates leukocyte circulation and extravasation from the blood into the areas of inflammation and macrophage differentiation [21–23]. The epithelial SIS3 molecular weight cells of adult colon do not normally express ICAM-1 which can be expressed subsequent to malignant transformation [24, 25]. ICAM-1 expression decreases CRC metastasis and suppress cancer progression via promoting tumor cell motility and attachment to the extracellular matrix [6]. The previous study has showed that expression level of ICAM-1 is high in well differentiated tumor cells and low levels in poorly
differentiated cells, and demonstrated a mechanism whereby ICAM-1 expression BMS-907351 cell line promotes CRC differentiation and retard metastasis [7]. ICAM-1 plays a role in promoting lymphocyte-mediated selleck chemicals tumor killing [26], and this occurs as a result of enhanced binding of peripheral blood mononuclear cells to the tumor cells and subsequent tumor cell lysis [27]. Yet the study suggests that ICAM-1 enhances tumor cell attachment to the extracellular matrix by promoting motility in the context of remodeling, and appears to be acting as a morphogen [7]. These findings provide a possible reason why increasing of ICAM-1 expression occurs in well differentiated
CRC tissues. Conclusion Our study herein provides a potential genetic factor for the differentiation of CRC that correlates with ICAM-1 K469E polymorphisms because of different ICAM-1 expression. However, we are unable to define the association of the ICAM-1 K469E polymorphisms with CRC risk owing to the limitations of the size of the CRC and control populations
in the present study. Our findings may help to evaluate the prognosis of CRC according to the individual genetic background. Acknowledgements The subject was supported by grants from National Natural Science Foundation of the People’s Republic of China (No. 30973820) and the Hebei Province Science and Technology Plan Programs of the People’s Republic selleck compound of China (No. 09276406D). References 1. Bahl R, Arora S, Nath N, Mathur M, Shukla NK, Ralhan R: Novel polymorphism in p21(waf1/cip1) cyclin dependent kinase inhibitor gene: association with human esophageal cancer. Oncogene 2000, 19: 323–328.CrossRefPubMed 2. Klintrup K, Makinen JM, Kauppila S, Vare PO, Melkko J, Tuominen H, Tuppurainen K, Makela J, Karttunen TJ, Makinen MJ: Inflammation and prognosis in colorectal cancer. Eur J Cancer 2005, 41: 2645–2654.CrossRefPubMed 3. Lichtenstein P, Holm NV, Verkasalo PK, Iliadou A, Kaprio J, Koskenvuo M, Pukkala E, Skytthe A, Hemminki K: Environmental and heritable factors in the causation of cancer–analyses of cohorts of twins from Sweden, Denmark, and Finland. N Engl J Med 2000, 343: 78–85.CrossRefPubMed 4.