期刊
JOURNAL OF CANCER
卷 13, 期 3, 页码 775-783出版社
IVYSPRING INT PUBL
DOI: 10.7150/jca.60417
关键词
cell growth; LINC01296; long non-coding RNA; migration and invasion; oral squamous cell carcinoma
类别
The study shows that LINC01296 is overexpressed in oral squamous cell carcinoma and is strongly associated with poor prognosis. LINC01296 may promote cancer cell growth, migration, and invasion through the regulation of the Wnt and MAPK signaling pathways. These findings suggest that LINC01296 could be a potential therapeutic target for oral squamous cell carcinoma.
Background: Oral squamous cell carcinoma (OSCC) is a common malignancy in the oral cavity that represents a significant global health problem. Multivariate analysis has shown that long non-coding RNA LINC01296 plays an important role in cancer biology. However, the functions of LINC01296 in OSCC are still unknown. Methods: The RNA profiles and clinicopathological information of OSCC patients and healthy subjects were downloaded. The expression level and prognostic value of LINC01296 were assessed. The functions and pathways of LINC01296were explored using the Gene Set Enrichment Analysis (GSEA) and functional analysis. The expression of LINC01296 in OSCC tissues and cell lines was determined by RT-qPCR. MTS assay was used to evaluate cell growth. The migration and invasion capacities of cells were assessed by wound healing assay and Transwell assay. Results: LINC01296 was overexpressed in the TCGA-OSCC datasets. High LINC01296expression was strongly correlated with poor outcomes of OSCC patients. LINC01296 was overexpressed in OSCC tissues compared with para-carcinoma tissues. Moreover, the expression of linc01296 was higher in CAL-27, HSC-2, and SCC-25 cells than in normal human oral keratinocytes (NHOKs). Functional analysis suggested that LINC01296might be involved in the regulation of the Wnt and MAPK signaling pathways. Additionally, LINC01296 deficiency suppressed the growth, migration, and invasion of OSCC cells, whereas overexpression of TFAP2A-AS1 cause opposite results. Conclusion: Our study showed that LINC01296 promoted OSCC cell growth, migration, and invasion, suggesting that LINC01296 might be a potential therapeutic target for OSCC.
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