RNA-binding protein CELF1 promotes tumor growth and alters gene expression in oral squamous cell carcinoma

The RNA binding protein CELF1 (also known as CUGBP1) is emerging as a critical regulator of cancer cell proliferation and apoptosis. Here, to provide a global prospective of CELF1 regulation of oral squamous cell carcinoma, we performed RNA-sequencing in oral cancer cells and CELF1 overexpression an...

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Bibliographic Details
Published in:Oncotarget 2015-12, Vol.6 (41), p.43620-43634
Main Authors: House, Reniqua P, Talwar, Sudha, Hazard, E Starr, Hill, Elizabeth G, Palanisamy, Viswanathan
Format: Article
Language:English
Subjects:
Animals
Blotting, Western
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - metabolism
Carcinoma, Squamous Cell - pathology
CELF1 Protein - metabolism
Cell Line
Gene Expression Regulation, Neoplastic - genetics
Head and Neck Neoplasms - genetics
Head and Neck Neoplasms - metabolism
Head and Neck Neoplasms - pathology
Heterografts
High-Throughput Nucleotide Sequencing
Humans
Immunoprecipitation
Male
Mice
Mice, Nude
Mouth Neoplasms - genetics
Mouth Neoplasms - metabolism
Mouth Neoplasms - pathology
Polymerase Chain Reaction
Research Paper
Squamous Cell Carcinoma of Head and Neck
Transcriptome
Transfection
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Summary:The RNA binding protein CELF1 (also known as CUGBP1) is emerging as a critical regulator of cancer cell proliferation and apoptosis. Here, to provide a global prospective of CELF1 regulation of oral squamous cell carcinoma, we performed RNA-sequencing in oral cancer cells and CELF1 overexpression analysis in non-malignant human oral keratinocytes. Our approaches identified 1283 mRNAs differentially regulated as a function of CELF1 expression and more importantly CELF1 promoted alternative splicing of several target pre-mRNAs, which are known to be involved in various cancer biological processes. Overexpression of CELF1 in non-malignant human oral keratinocytes protected cells against oxidative damage and altered gene expression patterns. Finally, we provide evidence that reduction of CELF1 protein using a xenograft tumorigenesis mouse model decreased tumor growth. Altogether, these data provided a comprehensive view of the CELF1 mRNA regulatory network in oral cancer and suggests that CELF1 and/or its target mRNAs are viable candidates for therapeutic intervention.
ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.6204