LncRNA EIF3J‐DT promotes chemoresistance in oral squamous cell carcinoma

Author:

Kim Seon Hyun1,Kim Hye Jung1ORCID,Kim Yeong Joo234,Kim Yun Hak134ORCID,Park Hae Ryoun15ORCID

Affiliation:

1. Periodontal Disease Signaling Network Research Center (MRC), School of Dentistry Pusan National University Yangsan Korea

2. Interdisciplinary Program of Genomic Data Science Pusan National University Yangsan Korea

3. Department of Anatomy, School of Medicine Pusan National University Yangsan Korea

4. Department of Biomedical Informatics, School of Medicine Pusan National University Yangsan Korea

5. Department of Oral Pathology, Dental & Life Science Institute, School of Dentistry Pusan National University Yangsan Korea

Abstract

AbstractObjectivesThis study aimed to screen oral squamous cell carcinoma (OSCC) diagnostic and prognostic candidates and investigate the potential functions and mechanisms of candidates in the chemoresistance of OSCC cell lines.Materials and MethodsDifferential expression profiling of lncRNA was performed in a large cohort of OSCC patients from the Cancer Genome Atlas database to identify OSCC diagnostic and prognostic candidates. Taxol resistance in OSCC cell lines was analyzed using MTT assay. OSCC cell lines transfected with EIF3J‐DT pcDNA or siRNA were used to determine its regulatory effects on apoptosis, cell cycle distribution and autophagy using flow cytometry and western blot.ResultsWe identified EIF3J‐DT as a candidate for OSCC diagnosis and prognosis. The expression level of EIF3J‐DT in OSCC cell lines correlates with taxol resistance. EIF3J‐DT silencing attenuated taxol resistance, and EIF3J‐DT overexpression enhanced taxol resistance in OSCC cell lines. Silencing of EIF3J‐DT reduced taxol resistance by inducing apoptosis, cell cycle arrest, and ATG14‐mediated autophagy inhibition in OSCC cell lines.ConclusionsWe found that EIF3J‐DT induced chemoresistance by regulating apoptosis, cell cycle, and autophagy in OSCC cell lines, which EIF3J‐DT might provide a novel therapeutic approach for OSCC as well as a diagnostic and prognostic factor.

Funder

National Research Foundation of Korea

Publisher

Wiley

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