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Hence, AKR1C3 emerges as a source of proliferative signals and a potential therapeutic target for both hormone-dependent and hormone-independent breast cancer (Byrns and Penning, 2009)

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Placental oxygen consumption

miR-155-5p downregulation enhances cell viability and inhibits apoptosis and ferroptosis Inhibition of miR-155-5p significantly increased cell viability and reduced apoptosis in KGN cells (Figure 5)