Journal
BIOENGINEERED
Volume 12, Issue 1, Pages 3978-3992Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2021.1948949
Keywords
Splicing factors; hepatocellular carcinoma; multi-omics; alternative splicing events
Categories
Funding
- Fund of National Natural Science Foundation of China [NSFC81860319]
Ask authors/readers for more resources
This study comprehensively investigated the genomic and epigenomic characteristics of SFs in HCC, revealing several clinically relevant SFs that could serve as effective biomarkers for monitoring the onset and prognosis of HCC. Copy number variation was found to be common in HCC, and the complex expression regulation of SFs was significantly affected by copy number variant and methylation. Furthermore, a potential regulatory network of SFs was identified, shedding light on their mechanisms in regulating clinically relevant alternative splicing events in HCC.
Splicing factors (SFs) have been increasingly documented to perturb the genome of cancers. However, little is known about the alterations of SFs in hepatocellular carcinoma (HCC). This study comprehensively delineated the genomic and epigenomic characteristics of 404 SFs in HCC based on the multi-omics data from the Cancer Genome Atlas database. The analysis revealed several clinically relevant SFs that could be effective biomarkers for monitoring the onset and prognosis of HCC (such as, HSPB1, DDX39A, and NELFE, which were the three most significant clinically relevant SFs). Functional enrichment analysis of these indicators showed the enrichment of pathways related to splicing and mRNA processes. Furthermore, the study found that SF copy number variation is common in HCC and could be a typical characteristic of hepato-carcinogenesis; the complex expression regulation of SFs was significantly affected by copy number variant and methylation. Several SFs with significant mutation patterns were identified (such as, RNF213, SF3B1, SPEN, NOVA1, and EEF1A1), and the potential regulatory network of SFs was constructed to identify their potential mechanisms for regulating clinically relevant alternative splicing events. Therefore, this study established a foundation to uncover the broad molecular spectrum of SFs for future functional and therapeutic studies of HCC.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available