{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:42:32Z","timestamp":1787013752346,"version":"build-2736575974"},"reference-count":39,"publisher":"Wiley","issue":"15","license":[{"start":{"date-parts":[[2025,8,9]],"date-time":"2025-08-09T00:00:00Z","timestamp":1754697600000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Thoracic Cancer"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Sortilin\u20101 (SORT1) has been implicated in the pathogenesis of various malignancies, but its role in non\u2010small cell lung cancer (NSCLC) remains to be elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Immunohistochemistry was employed to assess the expression of SORT1 in cancerous tissues compared to adjacent non\u2010cancerous tissues. NSCLC cell lines, including A549, H1299, and PC\u20109, underwent treatment with miR\u2010146a mimics or SORT1 small interfering RNA (siRNA), followed by evaluations of cell viability, migration, invasion, and apoptosis using cell counting kit\u20108, transwell assays, and scratch wound assays. Additionally, bioinformatic methods were employed to predict miR\u2010146a target genes, which were subsequently validated through dual\u2010luciferase reporter assays.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>SORT1 was significantly elevated in NSCLC tissues compared to adjacent non\u2010cancerous counterparts. Downregulation of SORT1 inhibited proliferation, invasion, migration of tumor cell lines and promoted apoptosis. Moreover, SORT1 was a direct target of miR\u2010146a. MiR\u2010146a modulated tumor cell proliferation, migration, invasion, and apoptosis by suppressing SORT1 expression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These results suggest that miR\u2010146a plays a critical role in the pathogenesis of NSCLC by targeting SORT1, highlighting its potential as a therapeutic target for NSCLC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/1759-7714.70129","type":"journal-article","created":{"date-parts":[[2025,8,9]],"date-time":"2025-08-09T08:18:21Z","timestamp":1754727501000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Sortilin\u20101, Targeted by\n                    <scp>miR<\/scp>\n                    \u2010146a, Regulates the Behavior of Non\u2010Small Cell Lung Cancer"],"prefix":"10.1111","volume":"16","author":[{"given":"Xi","family":"Lin","sequence":"first","affiliation":[{"name":"Department of Thoracic Surgery the Affiliated Hospital of Inner Mongolia Medical University  Hohhot China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi","family":"Yan","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine the Affiliated Hospital of Inner Mongolia Medical University  Hohhot China"},{"name":"Key Laboratory for Biomarkers Inner Mongolia Medical University  Hohhot China"},{"name":"School of Medical Laboratory Tianjin Medical University  Tianjin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Hai","sequence":"additional","affiliation":[{"name":"Department of Pathology Basic Medical College, Inner Mongolia Medical University  Hohhot China"},{"name":"Department of Pathology the Affiliated Hospital of Inner Mongolia Medical University  Hohhot 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