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HnRNP L is important for the expression of oncogene SRSF3 and oncogenic potential of oral squamous cell carcinoma cells.

ABSTRACT: Oral squamous cell carcinoma (OSCC) is the leading cause of death related to oral diseases. The mechanisms of OSCC development remain largely unknown. Heterogeneous nuclear ribonucleoprotein L (HnRNP L) is a multi-functional splicing factor. It has been reported to be an important regulator of apoptosis. However, the functions of hnRNP L in cancer need to be further explored. In the present study, we found that OSCC tissues expressed significantly higher levels of hnRNP L than normal tissues. Depletion of hnRNP L retarded cell growth, cell migration, and tumorigenesis of OSCC cells. HnRNP L regulates both the expression of oncogenic splicing factor SRSF3 and the alternative splicing of SRSF3 exon 4. Expression of hnRNP L is correlated with SRSF3 expression in OSCC tissues. These findings suggest that hnRNP L is important for the pathogenesis of OSCC and may be a novel potential therapeutic target of OSCC.

SUBMITTER: Jia R

PROVIDER: S-EPMC5093901 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature

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HnRNP L is important for the expression of oncogene SRSF3 and oncogenic potential of oral squamous cell carcinoma cells.

Jia Rong R Zhang Si S Liu Miaomiao M Zhang Yan Y Liu Yu Y Fan Mingwen M Guo Jihua J

Scientific reports 20161103

Oral squamous cell carcinoma (OSCC) is the leading cause of death related to oral diseases. The mechanisms of OSCC development remain largely unknown. Heterogeneous nuclear ribonucleoprotein L (HnRNP L) is a multi-functional splicing factor. It has been reported to be an important regulator of apoptosis. However, the functions of hnRNP L in cancer need to be further explored. In the present study, we found that OSCC tissues expressed significantly higher levels of hnRNP L than normal tissues. De ...[more]

PMID: 27808105

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Expression of SRSF3 is Correlated with Carcinogenesis and Progression of Oral Squamous Cell Carcinoma.

Project description:ObjectiveOral squamous cell carcinoma (OSCC) is the most common malignancy of head and neck with high mortality rates. The mechanisms of initiation and development of OSCC remain largely unknown. Dysregulated alternative splicing of pre-mRNA has been associated with OSCC. Splicing factor SRSF3 is a proto-oncogene and overexpressed in multiple cancers. The aim of this study was to uncover the relationship between SRSF3 and carcinogenesis and progression of oral squamous cell carcinoma.Design and methodsThe expression of SRSF3 in oral normal, dysplasia, or carcinoma tissues was analyzed by immunohistochemistry. The expression levels of EMT-related genes were quantified by real-time quantitative RT-PCR. The expression of SRSF3 in DMBA treated primary cultured oral epithelial cells were analyzed by western blot.ResultSRSF3 is overexpressed in oral cancer and moderate or severe dysplasia tissues. Patients with high grade cancer or lymphatic metastasis showed up-regulated expression of SRSF3. Knockdown of SRSF3 repressed the expression of Snail and N-cadherin in vitro. Carcinogen DMBA treated primary cultured oral epithelial cells showed significantly increased SRSF3 level than in control cells.ConclusionOur results suggested that SRSF3 is associated with the initiation and development of OSCC and may be a biomarker and therapeutic target of OSCC.

| S-EPMC4946124 | biostudies-literature

Inclusion of hnRNP L Alternative Exon 7 Is Associated with Good Prognosis and Inhibited by Oncogene SRSF3 in Head and Neck Squamous Cell Carcinoma.

Project description:Background and Objectives:Alternative 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 Methods:The 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. Results:The 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. Conclusions:Inclusion of hnRNP L alternative exon 7 is associated with good prognosis and inhibited by oncogene SRSF3 in HNSCC.

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Effects of hnRNP A1 on gene expression in oral squamous cell carcinoma

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Effects of hnRNP A1 on gene expression in oral squamous cell carcinoma

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| S-EPMC4880905 | biostudies-other

Oncogenic role of MiR-130a in oral squamous cell carcinoma.

Project description:Aberrant activation of the PI3K/AKT/mTOR pathway is attributed to the pathogenesis of oral squamous cell carcinoma (OSCC). In recent years, increasing evidence suggests the involvement of microRNAs (miRNAs) in oral carcinogenesis by acting as tumor suppressors or oncogenes. TSC1, as a component of the above pathway, regulates several cellular functions such as cell proliferation, apoptosis, migration and invasion. Downregulation of TSC1 is reported in oral as well as several other cancers and is associated with an unfavourable clinical outcome in patients. Here we show that oncogenic miR-130a binds to the 3'UTR of TSC1 and represses its expression. MiR-130a-mediated repression of TSC1 increases cell proliferation, anchorage independent growth and invasion of OSCC cells, which is dependent on the presence of the 3'UTR in TSC1. We observe an inverse correlation between the expression levels of miR-130a and TSC1 in OSCC samples, suggesting that their interaction is physiologically relevant. Delivery of antagomiR-130a to OSCC cells results in a significant decrease in xenograft size. Taken together, the findings of the study indicate that miR-130a-mediated TSC1 downregulation is not only a novel mechanism in OSCC, but also the restoration of TSC1 levels by antagomiR-130a may be a potential therapeutic strategy for the treatment of OSCC.

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CLPTM1L Is a Novel Putative Oncogene Promoting Tumorigenesis in Oral Squamous Cell Carcinoma.

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