越来越多的证据表明癌症治疗失败可归因于癌症干细胞（CSC）。在众多癌症干性调节因子中，非编码RNA（ncRNA）最近引起了极大的关注。在本研究中，我们检测了胃腺癌预测长基因间非编码RNA (GAPLINC)在口腔CSC (OCSC)中的作用。RNA测序和定量实时聚合酶链反应(qRT-PCR)用于测定GAPLINC的表达。利用流式细胞术和成球测定来分离 OCSC。在两种类型口腔癌细胞（SAS 和 GNM）的 CSC 中进行乙醛脱氢酶 1 (ALDH1) 活性、CD44 表达细胞的测量以及各种表型测定，例如自我更新、迁移、侵袭和集落形成能力。 ) 击倒 GAPLINC 后。还进行了荧光素酶报告基因验证 GAPLINC 和 microRNA (miR)-331-3p 之间的直接相互作用。我们的结果表明 GAPLINC 在来自患者来源和口腔癌细胞系的 OCSC 中过表达。我们证明，在 OCSC 中沉默 GAPLINC 会下调各种 CSC 标志，例如 ALDH1 活性、表达 CD44 的细胞百分比、自我更新能力和集落形成能力。此外，我们的结果表明，GAPLINC 对癌症干性的影响是通过直接抑制 miR-331-3p 介导的。这些数据具有潜在的临床意义，因为我们揭示了 GAPLINC 的异常上调，并证明抑制 GAPLINC 可能会降低癌症干性通过隔离 miR-331-3p。© 2024 中华民国牙科科学协会。 Elsevier B.V. 的出版服务

Accumulating evidence has suggested that treatment failure of cancer therapy can be attributed to cancer stem cells (CSCs). Among numerous regulators of cancer stemness, non-coding RNAs (ncRNAs) have gained significant attention recently. In this study, we examined the role of gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC) in oral CSCs (OCSCs).RNA Sequencing and quantitative real-time polymerase chain reaction (qRT-PCR) were used to determine the expression of GAPLINC. Flow cytometry and sphere-forming assay were exploited to isolate OCSCs. Measurement of aldehyde dehydrogenase 1 (ALDH1) activity, CD44 expressing cells, and various phenotypic assays, such as self-renewal, migration, invasion, and colony-forming abilities, were conducted in CSCs of two types of oral cancer cells (SAS and GNM) following the knockdown of GAPLINC. A luciferase reporter was also carried out to validate the direct interaction between GAPLINC and microRNA (miR)-331-3p.Our results showed that GAPLINC was overexpressed in OCSCs from patient-derived and oral cancer cell lines. We demonstrated that silencing of GAPLINC in OCSCs downregulated various CSC hallmarks, such as ALDH1 activity, percentage of CD44-expressing cells, self-renewal capacity, and colony-forming ability. Moreover, our results revealed that the effect of GAPLINC on cancer stemness was mediated by direct repression of miR-331-3p.These data have potential clinical implications in that we unraveled the aberrant upregulation of GAPLINC and demonstrated that suppression of GAPLINC may reduce cancer stemness via sequestering miR-331-3p.© 2024 Association for Dental Sciences of the Republic of China. Publishing services by Elsevier B.V.