LINC01296 promotes cancer stemness traits in oral carcinomas by sponging miR-143

Background/purpose: Emerging evidence has shown that various failures in cancer therapy, such as drug resistance, metastasis, and cancer relapse are attributed to cancer stem cells (CSCs). Also, growing attention has been paid to the regulation of non-coding RNAs in can-cer stemness. Here, we aimed to investigate the contribution of LINC01296 in the modulation of oral CSCs.Materials and methods: The phenotypic assays including migration, invasion, and colony -forming abilities were carried out in CSCs of two types of oral cancer cells (SAS and GNM) following the knockdown of LINC01296. In addition, the percentage of cells expressing stem-ness marker, ALDH1, and drug resistance marker, ABCG2, was examined as well as the self -renewal capacity after silencing of LINC01296. Moreover, a luciferase reporter was used to validate the direct interaction between LINC01296 and miR-143. Results: Our results showed that LINC01296 was significantly overexpressed in oral cancer tis-sues and positively correlated with stemness markers. The phenotypic and flow cytometry as-says demonstrated that suppression of LINC01296 reduced the aggressiveness, cancer stemness features, and colony-forming and self-renewal abilities in oral CSCs. Furthermore, we demon-strated that LINC01296 may enhance cancer stemness features through suppression of the ef-fect of miR-143.Conclusion: Silencing of LINC01296 may be a promising direction for oral cancer therapy by reducing cancer stemness via regulation of miR-143.(c) 2023 Association for Dental Sciences of the Republic of China. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons. org/licenses/by-nc-nd/4.0/).