{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T17:35:08Z","timestamp":1787765708424,"version":"build-2784847793"},"reference-count":39,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T00:00:00Z","timestamp":1758758400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[2025,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Gastric cancer (GC) is one of the most common cancers worldwide. Cancer cell metastasis is a major factor leading to poor prognosis. Previous proteomic data suggested that SSR4 might be closely associated with the occurrence and development of GC. However, the role and molecular mechanism of SSR4 in GC is not yet clear. The present study found that the expression level of SSR4 was increased in GC tissue and serum from GC patients. In addition, SSR4 could promote the malignant biological behavior of GC cells in vitro and in vivo. The mechanism may be that SSR4 regulates the expression of NDUFB11 and ATP6AP1, and then enhanced the function of mitochondrial respiratory chain complex I (CI) and mitochondrial respiratory chain complex V (CV), which promoted the mitochondrial oxidative phosphorylation and thus promoted GC progression. These findings expand the understanding of the role of SSR4 and provide a new target for the treatment of GC.<\/jats:p>","DOI":"10.1002\/mc.70047","type":"journal-article","created":{"date-parts":[[2025,9,26]],"date-time":"2025-09-26T03:48:37Z","timestamp":1758858517000},"page":"2026-2036","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["SSR4 Promote Gastric Cancer Progression by Regulating Mitochondrial Oxidative Phosphorylation via NDUFB11 and ATP6AP1"],"prefix":"10.1002","volume":"64","author":[{"given":"Aoshuang","family":"Li","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, The Third People's Hospital of Chengdu Affiliated Hospital of Southwest Jiaotong University Chengdu China"},{"name":"College of Medicine Southwest Jiaotong University Chengdu 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