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        <identifier>oai:figshare.com:article/34027713</identifier>
        <datestamp>2026-09-29T21:46:58Z</datestamp>
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          <dc:title>Apigenin ovarian cancer</dc:title>
          <dc:creator>Kwon (23828704)</dc:creator>
          <dc:subject>Signal transduction</dc:subject>
          <dc:subject>Cancer-stroma crosstalk</dc:subject>
          <dc:subject>Ovarian cancer cells</dc:subject>
          <dc:subject>Apigenin</dc:subject>
          <dc:subject>TGF-B signaling</dc:subject>
          <dc:subject>Fibroblasts</dc:subject>
          <dc:subject>AKT inhibition</dc:subject>
          <dc:description>&lt;p dir="ltr"&gt;Among stromal cells, fibroblasts serve as a major source of TGF-β1, which promotes ovarian cancer cell proliferation. However, TGF-β1-induced growth enhancement requires AKT activation in ovarian cancer cells, either through intrinsic constitutive hyperactivation or external fibroblast-derived factors other than TGF-β1. Furthermore, AKT activation is important for producing or maintaining TGF-β1 in fibroblasts. Among the polyphenols tested, apigenin effectively inhibited TGF-β1 secretion from fibroblasts and suppressed their pro-proliferative effects on ovarian cancer cells. Apigenin inhibited AKT activation in cancer cells and fibroblasts. In fibroblasts, apigenin-mediated AKT inhibition reduced the secretion of TGF-β1 available to promote cancer cell growth, whereas in ovarian cancer cells, apigenin reduced AKT-dependent proliferation, which functions as an intrinsic driver of cell proliferation and a permissive condition for TGF-β1-induced growth.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-29T21:46:58Z</dc:date>
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          <dc:identifier>10.6084/m9.figshare.34027713.v1</dc:identifier>
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