{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T05:59:56Z","timestamp":1790315996031,"version":"4.1.0"},"reference-count":62,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T00:00:00Z","timestamp":1790294400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Multidrug resistance remains a major barrier to effective chemotherapy for leukemia. Natural product-derived interventions have been widely investigated as modulators of drug resistance in adriamycin- or doxorubicin-resistant K562 cell models, but their quantitative reversal effects remain heterogeneous.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      <jats:italic>In vitro<\/jats:italic>\n                      studies evaluating natural product-derived interventions in resistant K562 leukemia sublines were synthesized. The primary meta-analytic endpoint was IC50-based reversal fold (RF), analyzed as log (RF) using an inverse-variance random-effects model. Subgroup, sensitivity, leave-one-out, and small-study-effect analyses were performed. Mechanistic outcomes related to transporter modulation, drug accumulation, apoptosis, and signaling pathways were summarized descriptively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Twenty-eight\n                      <jats:italic>in vitro<\/jats:italic>\n                      studies were included, and 19 IC50-based study-level effects were entered into the primary meta-analysis. The pooled RF was 6.31 (95% CI: 4.77\u20138.36), representing an overall chemosensitization signal across the restricted quantitative dataset. Subgroup analysis showed pooled RF values of 5.71 for K562\/A02, 4.90 for K562\/ADM, and 8.91 for K562\/ADR. Heterogeneity was high (I\n                      <jats:sup>2<\/jats:sup>\n                      = 97.7%), indicating substantial variability across resistant-cell sublines, intervention types, substrate drugs, and experimental conditions. Sensitivity analyses confirmed that the pooled effect remained positive, although exclusion of high-effect studies reduced the pooled RF to 4.51. Trim-and-fill analysis produced an adjusted pooled RF of 5.48 (95% CI: 3.87\u20137.76). Across individual studies, reported mechanisms included ABC transporter modulation, increased intracellular anthracycline accumulation, reduced efflux, restoration of apoptosis, and modulation of PI3K\/Akt, NF-\u03baB, and Nrf2\/ARE signaling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Across the heterogeneous studies, the common IC50-based endpoint showed an overall chemosensitization signal; however, this pooled summary does not imply a shared pharmacological action or potency across chemically distinct metabolites. Effect magnitude and mechanisms remained specific to individual metabolites, resistant-cell sublines, substrate drugs, doses, and molecular targets.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1892591","type":"journal-article","created":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T05:32:19Z","timestamp":1790314339000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Natural product-derived interventions for reversing multidrug resistance in resistant K562 leukemia cells: a systematic review and meta-analysis"],"prefix":"10.3389","volume":"17","author":[{"given":"Jingyi","family":"Sun","sequence":"first","affiliation":[{"name":"School of Biomedical and Chemical Engineering, Liaoning Institute of Science and Technology","place":["Benxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changning","family":"Song","sequence":"additional","affiliation":[{"name":"School of Biomedical and Chemical Engineering, Liaoning Institute of Science and Technology","place":["Benxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yining","family":"Hua","sequence":"additional","affiliation":[{"name":"School of Biomedical and Chemical Engineering, Liaoning Institute of Science and Technology","place":["Benxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiayin","family":"Pang","sequence":"additional","affiliation":[{"name":"School of Biomedical and Chemical Engineering, Liaoning Institute of Science and Technology","place":["Benxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuaiting","family":"Sun","sequence":"additional","affiliation":[{"name":"School of Biomedical and Chemical Engineering, Liaoning Institute of Science and Technology","place":["Benxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,25]]},"reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"78","DOI":"10.14715\/cmb\/2019.65.1.14","article-title":"Schizandrol A reverses multidrug resistance in resistant chronic myeloid leukemia cells K562\/A02","volume":"65","author":"Arken","year":"2019","journal-title":"Cell. 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