ArticleBioMed research international2019
Inclusion of hnRNP L Alternative Exon 7 Is Associated with Good Prognosis and Inhibited by Oncogene SRSF3 in Head and Neck Squamous Cell Carcinoma.
Article in BioMed research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- The role of splicing factor SRSF3 in cancer progression: Mechanisms, biomarkers, and therapeutic implications.Translational oncology · 2026Review
- Nonsense-mediated mRNA decay and associated splicing patterns in neurodevelopmental disorders.Frontiers in molecular biosciences · 2026Review
- The role of alternative pre-mRNA splicing in cancer progression.Cancer cell international · 2023Review
- FOXM1a Isoform of Oncogene FOXM1 Is a Tumor Suppressor Suppressed by hnRNP C in Oral Squamous Cell Carcinoma.Biomolecules · 2023Article
- SRSF3-Mediated Ki67 Exon 7-Inclusion Promotes Head and Neck Squamous Cell Carcinoma Progression via Repressing AKR1C2.International journal of molecular sciences · 2023Article
- Article
- Emerging roles of alternative RNA splicing in oral squamous cell carcinoma.Frontiers in oncology · 2022Review
- Article
- hnRNP A1B, a Splice Variant ofFrontiers in neuroscience · 2021Article
- Emerging Roles of SRSF3 as a Therapeutic Target for Cancer.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesAlternative splicing is increasingly associated with cancers. HnRNP L is a splicing factor that promotes carcinogenesis in head and neck squamous cell carcinoma (HNSCC) and other cancers. Alternative exon 7 of hnRNP L contains an in-frame stop codon. Exon 7-included transcripts can be degraded via nonsense-mediated decay or encode a truncated hnRNP L protein. Exon 7-excluded transcripts can encode full-length functional hnRNP L protein. HnRNP L has an autoregulation mechanism by promoting the inclusion of its own exon 7. This study aimed to understand the relationship between the alternative splicing of exon 7 and HNSCC. Oncogenic splicing factor SRSF3 has an alternative exon 4 and similar autoregulation mechanism. HnRNP L promotes SRSF3 exon 4 inclusion and then inhibits SRSF3 autoregulation. MATERIALS AND
methodsThe relationship between alternative splicing of hnRNP L exon 7 and clinical characteristics of HNSCC in a TCGA dataset was analyzed and confirmed by RT-PCR in a cohort of 61 oral squamous cell carcinoma (OSCC) patients. The regulators of exon 7 splicing were screened in 29 splicing factors and confirmed by overexpression or silencing assay in HEK 293, CAL 27, and SCC-9 cell lines.
resultsThe inclusion of hnRNP L exon 7 was significantly negatively associated with the progression and prognosis of HNSCC, which was confirmed in the cohort of 61 OSCC patients. SRSF3 inhibited exon 7 inclusion and hnRNP L autoregulation and then promoted the expression of full-length functional hnRNP L protein. SRSF3 exon 4 inclusion was correlated with hnRNP L exon 7 inclusion in both HNSCC and breast cancer. HNSCC patients with both low hnRNP L exon 7 and SRSF3 exon 4 inclusion show poor overall survival.
conclusionsInclusion of hnRNP L alternative exon 7 is associated with good prognosis and inhibited by oncogene SRSF3 in HNSCC.
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