Gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC) promotes oral cancer stemness by acting as a molecular sponge of miR331-3p

IF 3.4 3区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Journal of Dental Sciences Pub Date : 2024-07-01 DOI:10.1016/j.jds.2024.04.031
Kuang-Yuan Liang , Ni-Yu Su , Hsiu-Pin Yang , Pei-Ling Hsieh , Chih-Yuan Fang , Lo-Lin Tsai , Yi-Wen Liao , Chia-Ming Liu , Cheng-Chia Yu
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Abstract

Background/purpose

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).

Materials and methods

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.

Results

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.

Conclusion

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.

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胃腺癌预测性长基因间非编码 RNA (GAPLINC) 通过充当 miR331-3p 的分子海绵促进口腔癌干细胞的形成
背景/目的 越来越多的证据表明,癌症治疗失败可归因于癌症干细胞(CSCs)。在癌症干细胞的众多调控因子中,非编码 RNA(ncRNA)近来受到了广泛关注。在这项研究中,我们研究了胃腺癌预测性长基因间非编码RNA(GAPLINC)在口腔CSCs(OCSCs)中的作用。材料与方法RNA测序和定量实时聚合酶链反应(qRT-PCR)用于确定GAPLINC的表达。流式细胞术和球形成试验用于分离口腔癌细胞。在敲除 GAPLINC 后,对两种口腔癌细胞(SAS 和 GNM)的 CSCs 进行了醛脱氢酶 1 (ALDH1) 活性、CD44 表达细胞和各种表型检测,如自我更新、迁移、侵袭和集落形成能力。我们的研究结果表明,GAPLINC 在患者来源的口腔癌细胞系和口腔癌细胞系的 OCSCs 中过表达。我们的研究结果表明,GAPLINC 在患者来源的口腔癌细胞系和口腔癌细胞系的 OCSCs 中过表达,而在 OCSCs 中沉默 GAPLINC 会降低各种 CSC 标志,如 ALDH1 活性、CD44 表达细胞百分比、自我更新能力和集落形成能力。结论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可通过封闭miR-331-3p降低癌症干性。
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来源期刊
Journal of Dental Sciences
Journal of Dental Sciences 医学-牙科与口腔外科
CiteScore
5.10
自引率
14.30%
发文量
348
审稿时长
6 days
期刊介绍: he Journal of Dental Sciences (JDS), published quarterly, is the official and open access publication of the Association for Dental Sciences of the Republic of China (ADS-ROC). The precedent journal of the JDS is the Chinese Dental Journal (CDJ) which had already been covered by MEDLINE in 1988. As the CDJ continued to prove its importance in the region, the ADS-ROC decided to move to the international community by publishing an English journal. Hence, the birth of the JDS in 2006. The JDS is indexed in the SCI Expanded since 2008. It is also indexed in Scopus, and EMCare, ScienceDirect, SIIC Data Bases. The topics covered by the JDS include all fields of basic and clinical dentistry. Some manuscripts focusing on the study of certain endemic diseases such as dental caries and periodontal diseases in particular regions of any country as well as oral pre-cancers, oral cancers, and oral submucous fibrosis related to betel nut chewing habit are also considered for publication. Besides, the JDS also publishes articles about the efficacy of a new treatment modality on oral verrucous hyperplasia or early oral squamous cell carcinoma.
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