{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T18:38:59Z","timestamp":1766083139890,"version":"3.48.0"},"reference-count":24,"publisher":"Public Library of Science (PLoS)","issue":"12","license":[{"start":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T00:00:00Z","timestamp":1766016000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Medical Science Research Project of Hebei Province","award":["20231361"],"award-info":[{"award-number":["20231361"]}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"\n Background<\/jats:title>\n \n PTPRCAP<\/jats:italic>\n (protein tyrosine phosphatase receptor C-associated protein) has been implicated in tumor suppression in several malignancies; however, its role in lung adenocarcinoma (LUAD) remains unclear. This study aimed to investigate the expression profile and functional significance of\n PTPRCAP<\/jats:italic>\n in LUAD.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Forty-five pairs of LUAD and adjacent non-tumor tissues were collected from patients undergoing surgery at Chengde Medical University Affiliated Hospital.\n PTPRCAP<\/jats:italic>\n mRNA and protein levels were quantified by RT-qPCR and immunohistochemistry (IHC), respectively, and correlated with clinicopathological features. A549 and H1299 LUAD cell lines and BEAS-2B normal bronchial epithelial cells were used for in vitro assays.\n PTPRCAP<\/jats:italic>\n was overexpressed via plasmid transfection (OE group) and compared with vector-transfected controls (Vector group). Functional assays included CCK-8 proliferation, scratch wound healing, Transwell migration\/invasion, and Annexin V-PE apoptosis assays. Apoptosis-related proteins (Bax, Bcl-2, and cleaved caspase-3) were evaluated by Western blot. The effect of overexpression PTPRCAP on tumor growth was observed through nude mouse xenografts.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n PTPRCAP<\/jats:italic>\n mRNA and protein levels were significantly lower in LUAD tissues than in adjacent non-tumor tissues (P\u2009<\u20090.05). Low PTPRCAP expression correlated with advanced TNM stage and poor differentiation (P\u2009<\u20090.05). In vitro,\n PTPRCAP<\/jats:italic>\n expression was markedly reduced in A549 and H1299 cells compared with BEAS-2B. Overexpression of\n PTPRCAP<\/jats:italic>\n significantly suppressed proliferation, migration, and invasion (P\u2009<\u20090.001), and increased apoptosis rates in both cell lines (P\u2009<\u20090.01). Mechanistically, PTPRCAP upregulation elevated pro-apoptotic Bax and cleaved caspase-3 while downregulating anti-apoptotic Bcl-2 (P\u2009<\u20090.05). In vivo xenograft experiments demonstrated that overexpression PTPRCAP inhibited tumor growth in nude mice (P\u2009<\u20090.001).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n PTPRCAP<\/jats:italic>\n is downregulated in LUAD and acts as a tumor suppressor by promoting apoptosis and inhibiting proliferation, migration, and invasion. These findings suggest\n PTPRCAP<\/jats:italic>\n as a potential therapeutic target for LUAD.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1371\/journal.pone.0337223","type":"journal-article","created":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T18:31:34Z","timestamp":1766082694000},"page":"e0337223","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":0,"title":["Overexpression of PTPRCAP inhibits biological function of lung adenocarcinoma through apoptosis 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