LINC01116 in the Progression of OSCC

Oesophageal cancer (OC) is a significant threat to human health and is the eighth most common type of cancer worldwide. The most common type of OC is oesophageal squamous cell carcinoma (OSCC), accounting for around 85% of cases. Despite improvements in early screening and detection, access to effective therapy for advanced stages of the disease remains limited, resulting in OC being the sixth most common cause of cancer-related deaths.

Long non-coding RNAs (lncRNAs) are a type of RNA that does not have the ability to code for proteins and plays important roles in various disease processes. LncRNAs are involved in critical biological processes, including chromatin remodeling, transcriptional activation or silencing, and can affect transcription by binding with protein-coding genes. Antisense lincRNAs, which have no protein-coding counterparts, may also affect transcription through base-pair complimentary means. Aberrant expression and functions of lncRNAs have been linked to the development of several types of cancer, including OSCC, and provide potential avenues for diagnosis, prognosis, and targeted therapy.

Now researchers from China have set out to investigate the role of a long non-coding RNA (LINC01116) in the progression of oral squamous cell carcinoma (OSCC). In vitro and in vivo experiments were conducted to explore the potential role of LINC01116 in OSCC. Gene set enrichment analysis (GSEA) was conducted to identify the gene sets with significant enrichment. In general, their study provides insight into the molecular mechanism underlying the progression of OSCC, which may lead to the development of novel therapeutic targets for OSCC treatment.

First, they found that LINC01116 was upregulated in OSCC tissues. Its expression also was positively correlated with tumor differentiation and more advanced T stage, suggesting that LINC01116 up-regulation was an early event in OSCC development. Functional studies demonstrated that LINC01116 promoted OSCC cell proliferation and migration in vitro. In general, their findings indicate that LINC01116 may serve as a promising therapeutic target for the treatment of OSCC.

So, LINC01116 was highly expressed in OSCC tissues and associated with poor prognosis in patients. What else did they notice? LINC01116 was also found to regulate epithelial-mesenchymal transition (EMT) and increase the migration and invasion of OSCC cells. Moreover, they determined that LINC01116 interacts with AGO1 mRNA and control its expression. Knockdown of AGO1 led to reduced cellular migration and invasion, similar to the effect observed when LINC01116 was silenced. These results suggested that LINC01116 may promote the progression of OSCC through the regulation of AGO1 and could be a potential therapeutic target for OSCC.