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Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing
Published on: July 5, 2019
Identification of a novel fusion gene, TRIM52-RACK1, in oral squamous cell carcinoma
Tao Pan1, Yong-Guo Li2, Ke-Yi Li2
1Key Lab of Precision Biomedicine & Department of Stomatology, Liaocheng People's Hospital, College of Stomatology, Shandong First Medical University, China.
Abstract:
Gene fusion is caused by the linkage of previously separate genes or sequences. Recently, an increasing number of novel fusion genes have been identified and associated with tumor progression, and several of them have been suggested as promising targets for tumor therapy. However, there are hardly any studies reporting the association of fusion genes with the progression of oral squamous cell carcinoma (OSCC). In this study, we identified a total of 11 fused genes in OSCC cells. We further analyzed the structure of one fused gene, TRIM52-RACK1, and detected its function in tumor progression in vitro. We found that TRIM52-RACK1 was caused by a deletion of 181,257,187-181,247,386 at 5q35.3 and it promoted OSCC cell proliferation, migration, and invasion. Therefore, TRIM52-RACK1 can be a promising target for tumor therapy in OSCC.
Insights
Researchers identified 11 novel gene fusions in oral squamous cell carcinoma (OSCC). The TRIM52-RACK1 fusion promotes OSCC progression, suggesting it as a potential therapeutic target for this cancer.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Gene fusions are increasingly recognized in cancer development and progression.
- Novel fusion genes are potential therapeutic targets.
- The role of gene fusions in oral squamous cell carcinoma (OSCC) progression is understudied.
Purpose of the Study:
- To identify novel gene fusions in oral squamous cell carcinoma (OSCC) cells.
- To investigate the functional role of the TRIM52-RACK1 fusion gene in OSCC progression.
- To evaluate TRIM52-RACK1 as a potential therapeutic target for OSCC.
Main Methods:
- Identification of gene fusions in OSCC cells using molecular techniques.
- Analysis of the genomic structure of the TRIM52-RACK1 fusion.
- In vitro functional assays to assess the impact of TRIM52-RACK1 on OSCC cell proliferation, migration, and invasion.
Main Results:
- Eleven fused genes were identified in OSCC cells.
- The TRIM52-RACK1 fusion gene results from a deletion at chromosomal location 5q35.3.
- TRIM52-RACK1 significantly promoted OSCC cell proliferation, migration, and invasion in vitro.
Conclusions:
- TRIM52-RACK1 is a novel oncogenic fusion gene in oral squamous cell carcinoma (OSCC).
- TRIM52-RACK1 plays a crucial role in promoting OSCC progression.
- TRIM52-RACK1 represents a promising therapeutic target for OSCC treatment.
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