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    <responseDate>2026-10-10T19:32:37Z</responseDate>
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    <identifier>10.57760/sciencedb.37542</identifier>
    <datestamp>2026-05-25T18:04:56Z</datestamp>
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  <dc:date>2026-05-25</dc:date>
  <dc:title>Pseudolaric acid B triggers ferroptosis via activating AMPK pathway in cervical cancer</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.37542</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>	Cervical cancer ranks as the fourth malignancy among women globally, posing a significant threat to female health. Pseudolaric acid B (PAB), a bioactive diterpenoid constituent isolated from Pseudolarix amabilis, inhibits tumor progression. However, the underlying mechanisms remains to be elucidated in cervical cancer, especially. In this work, we aimed to investigate the effects of PAB in cervical cancer and explored its underlying mechanisms in vitro. PAB inhibited viability and proliferation of cervical cancer cells. PAB slightly induced apoptotic cell death although since it only triggerred modest cleavage of PARP and Caspase-3, without significant change the expression of Bcl-2 family. Furthermore, we found that PAB triggered ferroptosis in cervical cancer cells because PAB markedly increased Fe2+ accumulation and lipid peroxidation, and the ferroptosis inhibitor deferoxamine (DFO) strongly attenuated PAB-induced cell death. Moreover, PAB greatly downregulated the expression of ferroptosis-related proteins, including GPX4 and SLC7A11. Mechanistically, PAB significantly increased AMP-activated protein kinase (AMPK) activities. Furthermore, inhibition of AMPK with Compound C not only counteracted PAB-induced anticancer effects but also restored the expression of ferroptosis-related proteins. Consistently, knockdown of AMPK with siRNA further supported its critical part in PAB-mediated anticancer effects. Overall, this work demonstrated that PAB-induced ferroptosis represented a potential strategy for the treatment of cervical cancer and revealed the molecular mechanism by which PAB promoted ferroptosis activation through AMPK pathway. These findings provide a robust scientific basis for the clinical application of PAB in the treatment of cervical cancer.</dc:description>
  <dc:subject>Cervical cancer; PAB; Ferroptosis; AMPK</dc:subject>
  <dc:creator>li yu qiong</dc:creator>
  <dc:rights>EMBARGO</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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