Background Abnormal miRNA expression was recently implicated in the metastasis of oral squamous cell carcinoma (OSCC) and with a poor prognosis. The initiation of the invasion‐metastasis cascade involves epithelial‐mesenchymal transition (EMT). Our aim was to clarify how miRNA, especially miR‐155‐5p misexpression contributes to OSCC metastasis through EMT. Methods We collected tumor samples from 73 subjects with OSCC. The samples were analyzed by quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR), and correlations between miR‐155‐5p levels and clinical characteristics were investigated. OSCC cell lines were analyzed by miRNA microarray and by transfection with a miR‐155‐5p mimic or inhibitor, followed by proliferation and wound‐healing migration assays. qRT‐PCR analyses of EMT makers in cells transfected with miR‐155‐5p inhibitor were performed. Results We found high miR‐155‐5p expression in tissue samples from subjects with OSCC that had metastasized to cervical lymph nodes. HSC‐3 cells also strongly expressed miR‐155‐5p. The epithelial marker E‐cadherin was strongly expressed in HSC‐3 cells transfected with miR‐155‐5p inhibitor, and we observed elevated SOCS1 and decreased STAT3 expression in these cells. Conclusions Our results suggest that miR‐155‐5p causes OSCC to metastasize, and could serve as a novel therapeutic target for OSCC.

MicroRNAs (miRNAs or miRs) play important roles in carcinogenesis. The miRNA, miR-205-5p, has been reported to suppress the growth of various types of tumor; however, its functional contribution to oral squamous cell carcinoma (OSCC) is not yet clear. Thus, this study was conducted to determine the miRNA expression signatures in OSCC and to investigate the functional role of miR‑205‑5p in OSCC cells. We measured miR‑205‑5p expression by RT-qPCR, and examined the function of miR‑205‑5p by transfecting a miR‑205‑5p mimic or inhibitor into OSCC cells and measuring cell proliferation, migration and invasiveness. Genes targeted by miR‑205‑5p were identified using the TargetScan database and verified by western blot analysis, luciferase reporter assay and ELISA. We found that miR‑205‑5p was significantly downregulated in OSCC cell lines and tissue specimens. Following transfection of miR‑205‑5p mimic or inhibitor into the cancer cell lines, miR‑205‑5p overexpression significantly suppressed cancer cell migration and invasion. We further demonstrated that miR‑205‑5p directly targeted and regulated the tissue inhibitor of metalloproteinases‑2 (TIMP‑2) gene. The silencing of TIMP‑2 suppressed cancer cell invasion and the activation of pro‑matrix metalloproteinase‑2 (pro‑MMP‑2). These results suggest that TIMP‑2 promotes tumor progression, and that miR‑205‑5p directly regulates TIMP‑2, thereby suppressing pro‑MMP‑2 activation and inhibiting OSCC cell invasiveness. Our data describing the pathways regulated by miR‑205‑5p provide new insight into the mechanisms responsible for OSCC development and metastasis.

The combined squamous cell carcinoma (SCC) with neuroendocrine (atypical carcinoid (AC)) tumor is extremely rare in the head and neck. We present here the first case of SCC with AC arising in the floor of the mouth of 65-year-old man. The tumor is comprised of two components of SCC and AC in the biopsy specimen. Neuroendocrine tumor component was classified as AC from the punctate necrosis and 2–10>/10 HPF. Immunohistochemical staining was HMW-CK/34B (+) and P63 (+) in SCC and synaptophysin (+) and CD56 (+) in AC. The pathological diagnosis of SCC with AC was made from both the morphological and immunological exam. Concurrent chemoradiotherapy was performed with radiotherapy 70.2 Gy and chemotherapy of CDDP and VP-16. Although the treatment effect was complete response both of primary tumor and of neck metastases, the recurrence of the primary tumor was after 6 months. Bilateral modified radical neck dissection and tumor resection of the floor of the mouth with reconstructive surgery of anterior lateral thigh free flap were performed. Although the primary and neck tumor did not recur, the multiple lung metastases and mediastinum lymph node metastases occurred at 6 months after surgery.

A typical carcinoid is extremely rare in the oral cavity. We here present a case of a typical carcinoid arising in the sublingual gland of a 62-year-old woman. The tumor was removed by primary excision with 10 mm surgical margins and submandibular dissection. Examination of the tumor showed medium-sized tumor cells that were positive for CD56 and chromogranin A, with no necrosis, and with a mitotic count less than 1/10 HPF. A pathological diagnosis of typical carcinoid was made from both morphological and immunological examinations. One year after excision surgery, there was no tumor recurrence or neck metastasis.

MicroRNAs (miRNAs) play an important role in carcinogenesis and cancer progression. The purpose of this study was to identify miRNAs associated with carcinoma function in OSCC and to investigate the potential role of the specific miRNAs. First, a comprehensive microarray analysis was performed, and miR-142-5p was identified as a candidate miRNA involved in OSCC. miR-142-5p has been reported to show high expression levels in cancer patients and to be involved in tumor growth and metastasis. However, the expression and function of miR-142-5p in oral squamous cell carcinoma (OSCC) are not fully characterized. We evaluated miR-142-5p expression in both OSCC-derived cell lines and primary OSCC tissues and performed functional analysis of miR-142-5p in OSCC-derived cell lines using mimics and inhibitors. miR-142-5p expression was up-regulated in OSCC tissues and OSCC cell lines. Overexpression of miR-142-5p significantly promoted the proliferation and invasion of OSCC cells. Bioinformatics analysis was performed using TargetScan to predict potential target sites that match the seed region of miR-142-5p. Phosphatase and tensin homolog deleted on chromo-some 10 (PTEN) was identified as a potential target and selected for further analysis. PTEN expression levels were down-regulated and AKT expression levels were up-regulated in miR-142-5p-overexpressing cells. We have shown that miR-142-5p targets the PTEN gene and is involved in cancer progression. Our results suggest that miR-142-5p is involved in the progression of OSCC by controlling the phosphatidylinositol 3-kinase (PI3K)/AKT pathway by targeting the PTEN gene. Our findings suggest that miR-142-5p may be a new target for the treatment of OSCC.