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. Author manuscript; available in PMC: 2017 Feb 15.
Published in final edited form as: Int J Cancer. 2015 Oct 27;138(4):901–911. doi: 10.1002/ijc.29823

Figure 3.

Figure 3

HPV16 VLP binding to and PsV infection of tumor cell lines is competitively inhibited by heparin. (a) Flow histograms of 2µg/ml AF488 VLPs bound to cells in the absence (black line) or presence (gray line) of 1mg/ml heparin (negative control, dashed line). Tumor cell lines tested: Cervical (HeLa, SiHa, C 33A, CaSki); Head and Neck (CAL-33, HSC-3, UPCI SCC-90, UPCI SCC-154); Melanoma (SK-MEL 2, SK-MEL 5, SK-MEL 28, UACC-62); Lung (NCI-H23, NCI-H322M, NCI-H460, NCI-H522); Ovarian (SK-OV-3, A2780, OVCAR-3, OVCAR-4); Uroepithelial (J82, RT112, T24, UMUC-5). (b) Dose response inhibition of binding using modified heparins and heparinases on SK-OV-3 (ovarian, solid black line), NCI-H460 (lung, solid gray line) and SK-MEL-2 (melanoma, dashed black line) (experiment performed in triplicate, data representative of two experiments). Dose response of heparin inhibition of PsV infection of (c) ovarian, (d) lung and (e) melanoma cancer cell line panels. Heparin concentration begins with 1mg/ml and is serially diluted three-fold (experiment performed in triplicate, data representative of two experiments).