{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T14:14:28Z","timestamp":1778249668068,"version":"3.51.4"},"reference-count":37,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T00:00:00Z","timestamp":1774569600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T00:00:00Z","timestamp":1774569600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Multidrug resistance (MDR) remains a major challenge in small cell lung cancer (SCLC), limiting the efficacy of chemotherapeutics like doxorubicin. This study investigates whether silencing cellular prion protein (PrP), a known MDR\u2010associated molecule, can enhance doxorubicin\u2010induced cell death in Adriamycin\u2010resistant H69AR cells. Quantitative RT\u2010PCR and immunocytochemistry were used to assess the expression of\n                    <jats:italic>PRNP<\/jats:italic>\n                    ,\n                    <jats:italic>CD44<\/jats:italic>\n                    ,\n                    <jats:italic>BAX<\/jats:italic>\n                    , and\n                    <jats:italic>BECN1<\/jats:italic>\n                    under various treatment conditions, including doxorubicin exposure and PrP knockdown via siRNA. Autophagic activity was evaluated using monodansylcadaverine (MDC) staining. PrP knockdown significantly reduced\n                    <jats:italic>PRNP<\/jats:italic>\n                    expression and modulated\n                    <jats:italic>CD44<\/jats:italic>\n                    mRNA levels, especially during doxorubicin co\u2010treatment. However, CD44 protein levels remained unchanged, suggesting post\u2010transcriptional regulation.\n                    <jats:italic>BAX<\/jats:italic>\n                    expression increased with doxorubicin and siRNA individually, but not in combination, indicating a PrP\u2010independent mechanism.\n                    <jats:italic>BECN1<\/jats:italic>\n                    expression and Beclin\u20101 protein levels were significantly elevated in all treatment groups, especially in siRNA\/doxorubicin combination. MDC staining confirmed increased autophagic vacuole formation in this group, indicating activation of Beclin\u20101\u2010mediated autophagy. In conclusion, PrP knockdown may sensitize resistant SCLC cells to doxorubicin and promote autophagy. These findings support PrP silencing as a promising strategy to reverse chemoresistance in SCLC.\n                  <\/jats:p>","DOI":"10.1002\/cbf.70201","type":"journal-article","created":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T10:30:03Z","timestamp":1774607403000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Targeting Prion Protein to Overcome Doxorubicin Resistance in SCLC"],"prefix":"10.1002","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6978-8404","authenticated-orcid":false,"given":"Fatih","family":"\u00c7\u00f6ll\u00fc","sequence":"first","affiliation":[{"name":"Molecular Biology Section, Department of Biology, Faculty of Engineering and Natural Sciences Manisa Celal Bayar University Yunusemre\u2010Manisa 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