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The increase in IGFBP-1 and -2 leads to secondary increases in circulating IGF-I binding capacity that results in high total IGF-I, but decreased IGF-I bioactivity ( Figure 4 )

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Our data highlight the oncogenic role of ACTL6A in GCs and indicate that inhibition of ACTL6A or GCLC could be a potential treatment strategy for GCs

Abundance represents the metabolite level difference between conditioned and virgin media (n = 3 technical replicates from one experiment)