{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T03:30:24Z","timestamp":1782444624422,"version":"3.54.5"},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2021,1,5]],"date-time":"2021-01-05T00:00:00Z","timestamp":1609804800000},"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":["Oral Diseases"],"published-print":{"date-parts":[[2022,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>The study was designed to explore the role of cancer susceptibility candidate 9 (CASC9) in salivary adenoid cystic carcinoma (SACC) (SACC\u201083 and SACC\u2010LM) cell malignant phenotypes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Colony formation assay was used to measure cell proliferation. Transwell assay was used to detect cell migration and invasion. Flow cytometry analysis was applied to determine cell cycle distribution and apoptosis. FISH assay revealed the subcellular location of CASC9.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Downregulation of CASC9 inhibited SACC cell proliferation, migration, and invasion, led to cell arrest at G0\/G1 phase, and facilitated cell apoptosis. In mechanism, CASC9 bound with microRNA 146b\u20105p (miR\u2010146b\u20105p) and negatively modulated miR\u2010146b\u20105p expression. MiR\u2010146b\u20105p directly targeted 3\u2019 untranslated region of ATP\u2010Citrate Lyase (ACLY) to degrade ACLY in SACC cells. CASC9 upregulated ACLY expression through competitively binding with miR\u2010146b\u20105p. Furthermore, rescue assays indicated that ACLY overexpression counteracted the effects triggered by CASC9 knockdown on cell proliferation, migration, invasion, and apoptosis in SACC cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>CASC9 facilitated the malignant phenotypes of SACC cells by the regulation of the miR\u2010146b\u20105p\/ACLY axis. These findings might lay foundation for SACC research.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/odi.13759","type":"journal-article","created":{"date-parts":[[2020,12,21]],"date-time":"2020-12-21T12:41:38Z","timestamp":1608554498000},"page":"352-363","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["CASC9 plays a role in salivary adenoid cystic carcinoma in vitro by upregulation of ACLY"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6866-2807","authenticated-orcid":false,"given":"Hongliang","family":"Xie","sequence":"first","affiliation":[{"name":"Department of Oral and Maxillofacial Surgery Stomatological Medical Center Shenzhen People's Hospital The First Affiliated Hospital of South University of Science and Technology The Second Clinical Medical College of Jinan University Shenzhen 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