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They found that the knockdown of endogenous IRS-1 significantly decreased PI3K/AKT signaling and this effect was similarly shown in BC cells with miR-148a or miR-152 overexpression leading to the inhibition of cell proliferation

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or i.g., and effectiveness within g-ng range) ratio (12, 13), it may be reasonably to assume that these therapy effects may indicate a likely role of BPC 157 in controlling, and then, counteracting one or more causative process(es)

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