ArticleBioengineered2021
Long non-coding RNA LINC01296 acts as a migration and invasion promoter in head and neck squamous cell carcinoma and predicts poor prognosis.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- The Emerging Role of Long Non-coding RNA 01296 in Human Malignancies.Current molecular medicine · 2025Review
- Unraveling the Pivotal Role of LncRNA DUXAP9 in Cancer: Current Progress and Future Perspectives.Current drug targets · 2025Review
- Yin Yang 1-Induced Long Noncoding RNA DUXAP9 Drives the Progression of Oral Squamous Cell Carcinoma by Blocking CDK1-Mediated EZH2 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- LINC01296 promotes cancer stemness traits in oral carcinomas by sponging miR-143.Journal of dental sciences · 2023Article
- Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA (lncRNAs) can participate in gene expression regulation. LINC01296 is abnormally expressed in different tumors and promotes tumorigenesis and development. However, the role of LINC01296 in head and neck squamous cell carcinoma (HNSCC) remains not entirely clear. Thus, to explore LINC01296 expression, biological function and potential mechanism in HNSCC, we used GEPIA and GEO database. QRT-PCR was used to detect the knockout efficiency by LINC01296 inhibition with siRNA. Transwell assay was used to detect the migration and invasion capacity of tumor cells. Then enrichment and immunophenotype correlation analyses were carried out to explore the LINC01296 mechanism in HNSCC. To investigate why LINC01296 was up-regulated in HNSCC, DNA methylation analysis was performed using the DiseaseMeth database. LINC01296 expression was notably up-regulated in HNSCC, which was associated with promoter hypomethylation. Also, it was positively correlated with the HNSCC pathological stage and patients with higher LINC01296 expression levels had a poor prognosis. LINC01296 silencing inhibits HNSCC cell migration and invasion. LINC01296 also participate in the HNSCC progression mainly through protein phosphorylation and microtubule-based process regulation. Overall, LINC01296 was highly expressed in HNSCC, promoted tumor cells' migration and invasion, and might be a potential diagnostic and prognostic marker in HNSCC patients.
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