{'fraction_non_alphanumeric': 0.035859820700896494, 'fraction_numerical': 0.019559902200488997, 'mean_word_length': 6.1395348837209305, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Induction of Anchorage Independent Growth and Angiogenesis by Tungsten Carbide‐Cobalt Nanoparticles

Powder mixtures of nano‐sized tungsten carbide‐cobalt(WC‐Co) have wide applications because of their hardness and toughness. WC‐Cois known to be associated with pulmonary injury and malignant diseases. In this study, we investigated anchorage independent growth and the angiogenic response after exposure to WC‐Co nanoparticles. The results showed that chronic exposure of BEAS‐2B cells with low dose (0.025μg/cm2) WC‐Co significantly induced cell transformation in soft agar. WC‐Co nanoparticles also induced angiogenesis as determined by the chicken chorioallantoic membrane (CAM) assay. Mechanistic studies indicated that WC‐Co nanoparticles stimulatedalteration of miR‐21, PDCD4, AP‐1, NF‐kB, VEGF, AKT and ERKs activities. Inhibition of ERKs with U0126 reversed WC‐Co‐induced PDCD4 inhibition, but inhibition of p38 with SB203580 did not. These results illustrate that exposure to WC‐Co nanoparticles induces acarcinogenic response by activating AKT‐VEGF, and AP‐1‐MAPKs signal pathways and the downstream molecules. This information may be useful for preventing potential damage from nanoparticle exposure in the future.