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Differences of miRNA expression associated with ΔNp63β overexpressing OSCC cell line SQUU-B

ABSTRACT: Recent reports have revealed that EMT is involved in cancer invasion and progression including oral squamous cell carcinoma (OSCC). Previously, we have also studied on the association of p63 gene, a homolog of the p53 tumor suppressor gene, with EMT in OSCC cells. Furthermore, we also demonstrated that down-regulation of ΔNp63 accompanied with EMT and that re-expression of ΔNp63β by stable cDNA transfection in OSCC cell lines reverted the EMT phenotype. However, the detail mechanisms of ΔNp63β-mediated EMT remain to be unclear. Recent studies have shown that several microRNAs (miRNAs) are also involved in EMT process of human cancer by targeting EMT-related transcription factors. We thus sought to identify responsible miRNA associated with ΔNp63β-mediated EMT using miRNA microarray analyses.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE94047 | GEO | 2017/06/01

SECONDARY ACCESSION(S): PRJNA368645

REPOSITORIES: GEO

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Project description:Carcinogenesis is a multistep process in which cells accumulate multiple genetic alterations, as they progress to a more malignant phenotype. It has been proposed that sequential accumulation of gene abnormalities in specific genes drives the transition from non-tumorous epithelia through preneoplastic lesion/benign tumor to cancer. Histologically, progression to invasive oral squamous cell carcinoma (OSCC) follows multistep ordered series beginning with mucosal epithelial cell hyperplasia, followed by dysplasia, carcinoma in situ and invasive carcinoma. It is therefore speculated that genetic alterations-mediated multistep carcinogenesis would be involved in OSCC development, but their detailed molecular mechanisms are unknown. Herein, we clarified the comprehensive gene expression patterns and carried out an enrichment analysis using DNA microarray data obtained from an OSCC pathological specimen, which consists of non-tumor region, carcinoma in situ lesion and invasive carcinoma lesion. Numerous numbers of gene expression and signal activation were altered in the OSCC development. Of them, the expression of p63 was increased and MEK/ERK-MAPK pathway was activated in carcinoma in situ lesion as well as in invasive carcinoma lesion. Immunohistochemical analyses revealed that p63 was initially upregulated in carcinoma in situ lesions and ERK was sequentially activated in invasive carcinoma lesions in OSCC specimens. ADP-ribosylation factor (ARF)-like 4c (ARL4C), the expression of which is reportedly induced by p63 and/or MEK/ERK-MAPK pathway in OSCC cells, has been shown to promote tumorigenesis. Immunohistochemically, in OSCC specimens, ARL4C was more frequently detected in tumor lesions, especially in invasive carcinoma lesions than in carcinoma in situ lesions. Additionally, ARL4C and phosphorylated ERK were merged at high frequency in invasive carcinoma lesions. Loss-of-function experiments using inhibitors and siRNAs revealed that p63 and EGFR-MEK/ERK-MAPK cooperatively induce ARL4C expression in OSCC cells. These results suggest that the stepwise activation of p63 and EGFR-MEK/ERK-MAPK contributes to OSCC tumor cell growth though regulation of ARL4C expression.

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Differences of miRNA expression associated with ΔNp63β overexpressing OSCC cell line SQUU-B

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