Mucoepidermoid carcinoma arising in Warthin’s tumor of the upper lip: a case report and review / 口腔疾病防治

Objective @#To provide a reference for the diagnosis and treatment of mucoepidermoid carcinoma arising in Warthin’s tumor of the lip by investigating the diagnosis, treatment and prognosis of the disease.@*Methods @# A case of mucoepidermoid carcinoma arising in Warthin’s tumor of lip was reported, including the clinical manifestation, treatment, pathological characteristics and prognosis. The related literature was also reviewed and analyzed.@*Results@# A painless mass on the left lip lasting more than one month was found. Resection of the left lip was performed. Pathological examination showed that the tumor was a hybridoma composed of mucoepidermoid carcinoma and Warthin’s tumor. There was no recurrence or distant metastasis after 34 months. To date, this type of disease has been rarely reported. After thorough resection, the prognosis and survival rate are promising in most cases, with no recurrence or metastasis.@*Conclusion@#Mucoepidermoid carcinoma in Warthin’s tumor of the lip is rare. Clinical manifestations, imaging features and histological examination are useful when diagnosing the disease. Thorough resection will reduce the risk of disease recurrence.

Enhanced antitumor effect of cisplatin in human oral squamous cell carcinoma cells by tumor suppressor GRIM­19.

Gene associated with retinoid­interferon­induced mortality 19 (GRIM­19) is a novel candidate tumor suppressor gene located on the human chromosome 19p13.1 region. Our previous study demonstrated that the upregulation of GRIM­19 in human oral squamous cell carcinoma (OSCC) cells significantly inhibited tumor cell growth in vitro and in vivo. In the present study, the combined effects of cationic liposome (LP)­mediated GRIM­19 gene (LP­pGRIM­19) and the low­dose chemotherapeutic drug, cisplatin (CDDP), on tumor cell growth in vitro and in vivo were examined, and the molecular mechanism of their mutual action was investigated by cell proliferation, colony formation, apoptosis, migration, invasion and western blotting assays in vitro, and a node nude tumor model. It was demonstrated that cationic LP­pGRIM­19 gene therapy sensitized the response of breast cancer cells to CDDP, and that LP­pGRIM­19 in combination with CDDP significantly induced apoptosis and inhibited proliferation, colony formation, migration and invasion of the cells, compared with CDDP treatment alone. In addition, systemic treatment with a combination of intravenous injection of LP­pGRIM­19 and intraperitoneal injection of low­dose CDDP into subcutaneous HSC3 human OSCC xenograft mice resulted in a significant inhibition of tumor growth (P<0.05). Further investigations indicated that the enhancement of CPPP­mediated antitumor effects by GRIM­19 may be associated with the upregulation of phosphorylated p53 and the downregulation of B cell lymphoma­2, cyclin D1, vascular endothelial growth factor, matrix metalloproteinase (MMP)­2 and MMP­9, the proteins of which are involved in the activation of signal transducer and activator of transcription 3. The results of the present study suggested that the combination of GRIM­19 gene therapy with low­dose CPPP­based chemotherapy may be a potent therapeutic strategy for the treatment of OSCC.

Upregulation of GRIM-19 suppresses the growth of oral squamous cell carcinoma in vitro and in vivo.

Constitutive activation of the signal transducer and activator of transcription 3 (STAT3) and its upregulation contribute to the progression and metastasis of several different tumor types. The gene associated with retinoid­interferon­induced mortality-19 (GRIM-19) is known to functionally interact with STAT3 and inhibit its transcriptional activity. It has been reported that upregulation of genes associated with GRIM-19 can significantly reduce the tumor growth of several types of tumors. However, little is known in regards to its role in oral squamous cell carcinoma (OSCC). In the present study, a recombinant eukaryotic expression plasmid carrying GRIM-19 was constructed to evaluate its effects on OSCC cancer growth. Upregulation of GRIM-19 in OSCC cells significantly inhibited cell proliferation, migration and invasion in vitro and suppressed tumor growth in vivo. Moreover, we found that upregulation of GRIM-19 reduced cyclin D1, Bcl-2, vascular endothelial growth factor (VEGF) and matrix metalloproteinase-2 (MMP-2) expression whose protein is involved in STAT3 activation. Taken together, these findings suggest that GRIM-19 plays an inhibitory role in the progression of OSCC, and contribute to the future development of STAT3-based gene therapeutic approaches for OSCC.