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Overexpression of AKR1C3 is believed to be involved in hormone-dependent breast cancer by catalyzing the conversion of 4-androstene-3,17-dione to testosterone, which functions as a substrate for the aromatase-mediated synthesis of 17β-estradiol [99,100]
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Endogenous inhibitors such as soluble gp130 (sgp130) function as decoy receptors for the IL-6/sIL-6R complex, thereby specifically obstructing trans-signaling while preserving classic signaling (48)
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