Direct measurements on CD24-mediated rolling of human breast cancer MCF-7 cells on E-selectin.
نویسندگان
چکیده
Tumor cell rolling on the endothelium plays a key role in the initial steps of cancer metastasis, i.e., extravasation of circulating tumor cells (CTCs). Identification of the ligands that induce the rolling of cells is thus critical to understanding how cancers metastasize. We have previously demonstrated that MCF-7 cells, human breast cancer cells, exhibit the rolling response selectively on E-selectin-immobilized surfaces. However, the ligand that induces rolling of MCF-7 cells on E-selectin has not yet been identified, as these cells lack commonly known E-selectin ligands. Here we report, for the first time to our knowledge, a set of quantitative and direct evidence demonstrating that CD24 expressed on MCF-7 cell membranes is responsible for rolling of the cells on E-selectin. The binding kinetics between CD24 and E-selectin was directly measured using surface plasmon resonance (SPR), which revealed that CD24 has a binding affinity against E-selectin (K(D) = 3.4 ± 0.7 nM). The involvement of CD24 in MCF-7 cell rolling was confirmed by the rolling behavior that was completely blocked when cells were treated with anti-CD24. A simulated study by flowing microspheres coated with CD24 onto E-selectin-immobilized surfaces further revealed that the binding is Ca(2+)-dependent. Additionally, we have found that actin filaments are involved in the CD24-mediated cell rolling, as observed by the decreased rolling velocities of the MCF-7 cells upon treatment with cytochalasin D (an inhibitor of actin-filament dynamics) and the stationary binding of CD24-coated microspheres (the lack of actins) on the E-selectin-immobilized slides. Given that CD24 is known to be directly related to enhanced invasiveness of cancer cells, our results imply that CD24-based cell rolling on E-selectin mediates, at least partially, cancer cell extravasation, resulting in metastasis.
منابع مشابه
Obligatory requirement of sulfation for P-selectin binding to human salivary gland carcinoma Acc-M cells and breast carcinoma ZR-75-30 cells.
Stimulated endothelial cells and activated platelets express P-selectin, which reacts with P-selectin glycoprotein ligand-1 (PSGL-1) for leukocyte rolling on the stimulated endothelial cells and heterotypic aggregation of the activated platelets on leukocytes. P-selectin also binds to several cancer cells in vitro and promotes the growth and metastasis of human colon carcinoma in vivo. The P-se...
متن کاملThe CD24/P-selectin binding pathway initiates lung arrest of human A125 adenocarcinoma cells.
Carbohydrates on tumor cells have been shown to play an important role in tumor metastasis. We demonstrated before that CD24, a Mr 35,000-60,000 mucine-type glycosylphosphatidylinositol-linked cell surface molecule, can function as ligand for P-selectin and that the sialylLex carbohydrate is essential for CD24-mediated rolling of tumor cells on P-selectin. To investigate the role of both antige...
متن کاملEvaluation of Stem Cell Markers, CD44/CD24 in Breast Cancer Cell Lines
Background Cancer stem cells play crucial roles in resistance to therapeutic schemes and relapse of disease, so it is important to find targeted therapies that kill them selectively. Breast cancer is the most common cancer in females living in all part of the world including Iran and it has an important burden in public health with direct impact on patients’ families. Breast cancer in young ad...
متن کاملThe Extracts of Epilobium Parviflorum inhibit MCF-7 Breast Cancer Cells
Background: Traditional medicine is inspiring in drug development research. Epilobium parviflorum extracts have shown promising therapeutic effects on prostate cancer cells. The similarities between breast and prostate cancers at molecular and metabolic levels prompted us to explore its effects on human breast cancer. Methods: The root, aerial parts and flowers of the plant were, collected and...
متن کاملSTAT3 mediates resistance of CD44+CD24−/low breast cancer stem cells to tamoxifen in vitro
We sought to determine whether STAT3 mediated tamoxifen resistance of breast cancer stem cells in vitro. The capacities for mammosphere formation and STAT3 expression of CD44(+)CD24(-/low) MCF-7 and MCF-7 were observed. The CD44(+)CD24(-/low) subpopulation ratio and its sensitivity to adriamycin were analyzed in MCF-7 and TAM resistant (TAM-R) cells. Cell cycle, apoptosis, STAT3 and phospho-STA...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Analytical chemistry
دوره 83 3 شماره
صفحات -
تاریخ انتشار 2011