Identifying Differences Between a Straight Face and a Posed Smile Using the Homologous Modeling Technique and the Principal Component Analysis.

Recently, a homologous modeling method was developed to simulate 3D human body forms, which can visualize principal component analysis (PCA) results and facilitate its detailed comparison with results of previous method. Herein, we aimed to construct a homologous model of the face to identify differences between a straight face and a posed smile. Thirty-eight volunteers (19 males and 19 females, 38 straight faces and 38 posed smiles) with no medical history associated with a posed smile were enrolled. Three-dimensional images were constructed using the Homologous Body Modeling software and the HBM-Rugle; 9 landmarks were identified on the 3D-model surfaces. The template model automatically fitted into an individually scanned point cloud of the face by minimizing external and internal energy functions. Faces were analyzed using PCA; differences between straight faces and posed smiles were analyzed using paired t tests. Contribution of the most important principal component was 23.8%; 8 principal components explained >75% of the total variance. A significant difference between a straight face and a posed smile was observed in the second and the fourth principal components. The second principal component images revealed differences between a straight face and a posed smile and changes around the chin area with regard to length, shape, and anteroposterior position. Such changes were inclusive of individual differences. However, the fourth principal component image only revealed differences between a straight face and a posed smile; observed differences included simultaneous shortening of upper and lower eyelid length, evaluation of the nasal ala ase, swelling of the cheek area, and elevation of the mouth angle. Although these results were clinically apparent, we believe that this article is the first to statistically verify the same.Consequently, the homologous model technique and PCA are useful for evaluation of the facial soft-tissue changes.

Targeting ID2 expression triggers a more differentiated phenotype and reduces aggressiveness in human salivary gland cancer cells.

Inhibitors of DNA-binding (ID) proteins are negative regulators of basic helix-loop-helix transcription factors and generally stimulate cell proliferation and inhibit differentiation. We previously determined that ID1 was highly expressed in aggressive salivary gland cancer (SGC) cells in culture. Here, we show that ID2 is also expressed in aggressive SGC cells. ID2 knockdown triggers important changes in cell behavior, that is, it significantly reduces the expression of N-cadherin, vimentin and Snail, induces E-cadherin expression and leads to a more differentiated phenotype exemplified by changes in cell shape. Moreover, ID2 knockdown almost completely suppresses invasion and the expression of matrix metalloproteinase 9. In conclusion, ID2 expression maintains an aggressive phenotype in SGC cells, and ID2 repression triggers a reduction in cell aggressiveness. ID2 therefore represents a potential therapeutic target during SGC progression. ID proteins are negative regulators of basic helix-loop-helix transcription factors and generally stimulate cell proliferation and inhibit differentiation. ID2 knockdown triggers important changes in cell behavior, that is, it significantly reduces the expression of N-cadherin, vimentin and Snail, induces E-cadherin expression and leads to a more differentiated phenotype exemplified by changes in cell shape. ID2 therefore represents a potential therapeutic target during SGC progression.

Targeting Id1 reduces proliferation and invasion in aggressive human salivary gland cancer cells.

BACKGROUND: Salivary gland cancer (SGC) is one of the common malignancies of the head and neck area. It develops in the minor and major salivary glands and sometimes metastasizes to other organs, particularly to the lungs. Inhibitors of differentiation (Id) proteins are negative regulators of basic helix-loop-helix transcription factors that control malignant cell behavior and tumor aggressiveness in many tissues. In this study, our goal was to determine the potential role of Id proteins, particularly Id1, during human SGC cell progression. METHODS: We first determined the expression levels of Id1 and Id2 in four SGC cell lines: two adenocarcinoma of the salivary gland (HSG and HSY) and two adenoid cystic carcinoma (ACC2 and ACCM) cell lines. We then used constructs that expressed antisense cDNAs to Id1 or Id2 to knockdown the expression of these proteins in cell lines where they were highly expressed, and determined the effects of the knockdown on cell proliferation, migration and invasion. RESULTS: Id1 mRNA and protein were detectable in all cell lines, and expression of Id2 was variable, from absent to high. The ACC2 and ACCM cell lines expressed both Id1 and Id2, but Id1 was expressed at a higher level in the more aggressive ACCM cell line in comparison to ACC2 cells as confirmed by Id1 promoter-reporter assays. We therefore focused on the ACCM cells for the remainder of the study. We found that proliferation and invasiveness of ACCM cells were strongly reduced after Id1 knockdown whereas Id2 suppression had only a slight effect. Results of scratch and colony formation assays also confirmed that ACCM cell aggressiveness was significantly reduced upon Id1 knockdown. Finally, this knockdown resulted in reduced c-myc and enhanced cyclin-dependent kinase inhibitor p21 expression. CONCLUSIONS: These results demonstrate that Id1 plays an important role in the control of human SGC cell aggressiveness and suggest a potential role as a marker of diagnosis, prognosis and progression of SGCs. Id1 suppression could represent a novel and effective approach for the treatment of salivary gland cancer.

Application of a new scan body for face-driven fixed prosthetics.

OBJECTIVE: The current method of digitally designing dental prostheses mainly focuses on intra-oral soft and hard tissues, although the harmony of the facial soft tissue and the prosthesis is crucial, especially for esthetics. Here, we introduce a new method of digitally designing dental prostheses using a new device that generates a virtual patient and incorporates facial features into the prosthetic design. MATERIALS AND METHODS: A new extra-oral scan body for facial scanning was designed and developed. A definitive edentulous maxilla implant cast with four extra-oral scan bodies (regions: maxillary left and right lateral incisors, maxillary left and right premolars) was placed in the mouth of a dental mannequin. The dental mannequin was scanned with and without the extra-oral scan bodies. For reference data, an impression of the maxilla was taken and scanned with a laboratory scanner. By superimposing each acquired data, a virtual patient was generated, and the spatial location of the abutments relative to the face was clarified. Identifying the accurate location of the abutments enabled to design face-driven dental prosthesis. RESULTS: Based on the color-coded deviation map created by the data acquired from conventional and extra-oral scan bodies, the divergence of the two data was mostly within 0.1 mm, which proves that the extra-oral scan bodies were as accurate as conventional scan bodies. Therefore, the facial scan data and the scan data of the oral cavity were successfully superimposed, which allowed to generate a virtual patient to design face-driven prosthesis. CONCLUSION: The new method is effective for designing high-quality face-driven prostheses, especially when treating a patient with a full-arch implant-fixed prosthesis.

Silencing Id-1 with RNA interference inhibits adenoid cystic carcinoma in mice.

BACKGROUND: The helix-loop-helix (HLH) protein Id-1 (inhibitor of DNA binding/differentiation) has been demonstrated to play an important role in tumor development. Our previous in vitro research has shown that Id-1 is a potential target in the treatment of human adenoid cystic carcinoma (ACCM). The purpose of this study was to analyze the influence of Id inhibition on ACCM in mice. MATERIALS AND METHODS: To suppress the expression of Id-1 gene, we used lentivirus-mediated RNA interference to silence the Id-1 gene post-transcriptionally in ACCM models that stably express GFP in mice. Tumor development was evaluated by size measurement. Effects of Id-1 siRNA on mRNA and protein expression of Id-1 were analyzed using quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting respectively. Ki-67 expression was measured by immunohistochemistry. In vitro studies of Hoechst staining for cell apoptosis, Boyden-chamber assay for cell invasion, and MTT-tests for cell growth were performed as well. RESULTS: Id-1 knockdown resulted in inhibition of tumor growth in mice. Id-1 siRNA significantly decreased not only Id-1 in mRNA and protein level, but also Ki-67 expression. In addition, apoptosis was induced and cell proliferation activity and invasion were significantly reduced. CONCLUSIONS: Lentivirus-mediated gene knockdown by silencing Id-1 constitute a valid methodological approach, which may represent an attractive, potent and specific therapeutic tool for the treatment of ACCM.

Massive subcutaneous emphysema developing before surgery for mandibular fracture: a case report.

Preoperative massive subcutaneous emphysema before intubation is extremely rare. However, this complication may be potentially lethal, depend on the condition of air spreading. Subcutaneous emphysema which occurs intra- or postoperative period is sometimes iatrogenic because the air is introduced into the tissue space through the hole injured by the operation. But the emphysema in this case occurred preoperatively by the pressure of the bag valve mask, because the patient had an intra-oral wound, which reaches the submental space. In this report, we describe an extremely rare case of preoperative massive emphysema of the patient with the mandibular fracture.

Lower Lip Cancer Managed by Reconstruction with a Double Abbe Flap - A Case Report.

Although the incidence of lower lip cancer is not high in Japan, its treatment requires an approach that considers both esthetics and function. When surgical resection is required, the method used for reconstruction varies depending on the affected part. Despite various studies proposing different types of algorithms, no single method is considered the best. If the loss of half or more of the lip is predicted, a free flap may need to be considered, depending on the case. Here, we report a case involving a 78-year-old edentulous woman with lower lip cancer whose resection area involved approximately 70% of the red and white portions of the lower lip. Fortunately, no resection was required at the commissure. We accordingly performed reconstruction with a double Abbe flap in accordance with a detailed treatment plan. The patient was extremely satisfied with the esthetic and functional outcomes of the surgery.

Beckwith-Wiedemann syndrome with asymmetric mosaic of paternal disomy causing hemihyperplasia.

Beckwith-Wiedemann syndrome (BWS) is a congenital disorder with 3 main features-overgrowth in infancy, macroglossia, and abdominal wall defects. Here, we report on a 5-month old girl with hemihyperplasia and macroglossia caused by paternal uniparental disomy (pUPD) asymmetric mosaic on chromosome 11p15.5. She could not retract her tongue into her mouth and the midline of the tongue was shifted to the left. Glossectomy was performed at age 1 year. A specimen of the tongue showed normal skeletal muscle, but the muscle fibers were closely spaced, and there were fewer stroma components in the tissue from the right side of the tongue than that from the left side. With respect to pUPD of chromosome 11p15.5, microsatellite marker analysis of the tongue tissue specimen revealed a higher mosaic rate in the tissue from the right side of the tongue (average 48.3%) than that from the left side (average 16.9%). Methylation analysis of Kv differentially methylated region (DMR) 1 (KvDMR1) and H19DMR revealed hypomethylation of KvDMR1 and hypermethylation of H19DMR in the tissue on the right side of the tongue (hyperplastic side). In this case, the difference in mosaic rate of pUPD in the 11p15.5 region was hypothesized to influence the expression level of insulin-like growth factor 2. This result may be helpful to clinicians, especially surgeons, when planning plastic surgery for hemihyperplasia.

Expression of Id and ITF-2 genes in the mammary gland during pregnancy.

Id-1 is one of the four related helix-loop-helix Id proteins that act as inhibitors of the basic helix-loop-helix (bHLH) transcription factors that control cell differentiation, development and carcinogenesis. We previously found that Id-1 regulated the growth, differentiation, apoptosis and invasion of mouse mammary epithelial cells in culture. Using the techniques of immunohistochemistry and in situ hybridization, we now show that Id-1 gene expression is specifically detected in the epithelial cells of growing ductal structures during early pregnancy. Using adjacent sections, we determined that Id-1 was expressed in keratin 8/18 positive cells. We also demonstrated that the up-regulation of Id-2 during late pregnancy correlated with the down-regulation of Id-1. Using the yeast-two hybrid system, we identified the bHLH transcription factors, ITF-2A and ITF-2B, as the Id-interacting proteins. The levels of expression of these two splice variants did not change during the transition from growing ductal structures to differentiated alveoli. Therefore Id-1 and Id-2, but not the ubiquitous bHLH proteins, appear to represent the key factors whose expression is modulated during different stages of pregnancy in mouse mammary glands.

Mandibular central leiomyosarcoma with high telomerase activity: a case report.

Leiomyosarcoma is a malignant lesion of smooth muscle origin, and rare in the oral region. This report presents an extremely rare case of intraosseous leiomyosarcoma of the mandible. After visiting other general hospital, a 29-year-old man was referred to our hospital because of a pain in the left mandibular region with paresthesia of the left mental region. The left mandibular third molar had already been extracted in another hospital, and a brownish mass occupied the corresponding region. A panoramic radiograph showed osteolytic destruction around the left mandibular angle and ramus. A computed tomography scan and magnetic resonance image revealed perforation of the lingual and buccal cortex of the mandible. A non-epithelial malignant tumor was diagnosed from a biopsy specimen. Immediately, we resected the tumor and reconstructed the titan plate under general anesthesia. A final diagnosis of leiomyosarcoma was made from a surgical specimen based on findings showing a proliferation of hyperchromatic spindle cells, which were positive for the markers α- smooth muscle actin, calponin, HHF35, and desmin. The S-100, epithelial membrane antigen, and cytokeratin markers were negative. The patient had 3 courses of adjuvant chemotherapy after the operation, and showed no evidence of recurrence during the follow-up at the outpatient clinic. However, 2 years after the first operation, lung metastases and local recurrence were detected. Additional chemotherapy was not effective. Finally, the patient died almost 3 years after the first operation.

Osteosynthesis Using the Uncalcined and Unsintered Hydroxyapatite / Poly-L-Lactic Acid System.

The poly-L-lactic acid mini-plate system accomplished rapid development. However, the system still has a variety of problems. One such problem is the breakage of screws. In this technical report, we develop the temporary fixing screws made from stainless with hexagon steel that exhibit a hexagonal head and thread part that also features a tapping function.

Deregulation of Nicotinamide N-Methyltransferase and Gap Junction Protein Alpha-1 Causes Metastasis in Adenoid Cystic Carcinoma.

BACKGROUND/AIM: Adenoid cystic carcinoma (AdCC) is a malignant tumor that occurs in the salivary glands and frequently metastasizes. The aim of this study was to identify factors mediating AdCC metastasis. MATERIALS AND METHODS: We established three AdCC cell lines by orthotropic transplantation and in vivo selection: parental, highly metastatic (ACCS-M-GFP), and lymph node metastatic (ACCS-LN-GFP) cells. RESULTS: We examined the three cell lines. DNA microarray indicated significantly altered processes in ACCS-LN-GFP cells: particularly, the expression of nicotinamide N-methyltransferase (NNMT) was enhanced the most. NNMT is associated with tumorigenesis and is a potential tumor biomarker. Concomitantly, we found-significant down-regulation of gap junction protein alpha-1. We suggest that ACCS-LN-GFP cells acquire cancer stem cell features involving the up-regulation of NNMT and the loss of gap junction protein alpha-1, leading to epithelial-mesenchymal transition and consequent AdCC metastasis. CONCLUSION: NNMT is a potential biomarker of AdCC.

Regulation of ß-Catenin Phosphorylation by PR55ß in Adenoid Cystic Carcinoma.

BACKGROUND/AIM: Adenoid cystic carcinoma (AdCC) is a rare cancer of the salivary gland with high risk of recurrence and metastasis. Wnt signalling is critical for determining tumor grade in AdCC, as it regulates invasion and migration. ß-catenin dephosphorylation plays an important role in the Wnt pathway, but its underlying molecular mechanism remains unclear. MATERIALS AND METHODS: Because the regulatory subunits of protein phosphatase 2A (PP2A) drive Wnt signalling via target molecules, including ß-catenin, we used qRT-PCR and immunoblot analysis to investigate the expression of these subunits in an AdCC cell line (ACCS) and a more aggressive subline (ACCS-M). RESULTS: PR55ß was highly expressed in ACCS-M, suggesting its functional importance. In addition, PR55ß expression was associated with tumor grade, with ACCS-M exhibiting higher PR55ß levels. More importantly, knockdown of PR55ß in ACCS-M cells significantly reduced invasiveness and metastatic ability. Furthermore, dephosphorylation and total levels of ß-catenin were dependent on PR55ß in ACCS-M. Finally, we confirmed a correlation between PR55ß staining intensity and histopathological type in human AdCC tissues. CONCLUSION: Our study provides new insight into the interaction between PR55ß and ß-catenin and suggests that PR55ß may be a target for the clinical treatment of AdCC.

The relationship between lateral displacement of the mandible and scoliosis.

OBJECTIVES: Idiopathic scoliosis is an orthopaedic disease of childhood, with onset and progress occurring until adolescence. Here, the relationship between lateral displacement of the mandible and scoliosis was analysed quantitatively. METHODS: Seventy-nine non-syndromic Japanese patients (18 men, 61 women), who were diagnosed with jaw deformities and underwent surgical orthognathic treatment at Kyushu University Hospital from January 2011 to August 2014, were enrolled. Their mean age at the time of radiography was 25.3 ± 8.7 years. Postero-anterior cephalometric radiographs and chest radiographs were examined. In postero-anterior cephalometric radiographs, a horizontal baseline (X-axis) was drawn as a straight line that intersects both the zygomatic bases, and a vertical line (Y-axis) was marked perpendicular to the X-axis, with an intersection at the anterior nasal spine (ANS). Point A was defined as the intersection of the X- and Y-axes, and line A was defined as the line connecting point A to the menton. The angle made by the X-axis and line A (i.e., lateral displacement of the mandible) was measured. We designated an absolute value even if the mandibular menton was located on the right or left side. In chest radiographs, Cobb's method was used to measure scoliosis curves; the direction of the curve was designated similarly. RESULTS: Nine (11.4%) individuals had a Cobb angle >10°. There was a positive correlation between the Cobb angle and the degree of mandibular deviation (p < 0.05). CONCLUSION: Lateral displacement of the mandible and scoliosis are related.

Reduction of human metastatic breast cancer cell aggressiveness on introduction of either form a or B of the progesterone receptor and then treatment with progestins.

The sex steroid hormone progesterone (Pg) is critically involved in the development of the mammary gland, and it also is thought to play a role in breast cancer progression. However, the effect of Pg on malignant phenotypes is not fully understood in breast cancer. We previously reported that in Pg receptor (PR)-positive T47D breast cancer cells, Pg was able to counterbalance the stimulatory effect of estrogen or serum on proliferation and on expression level of Id-1, which generally stimulates cell proliferation and inhibits differentiation. Conversely, metastatic MDA-MB231 breast cancer cells lack PR and express high levels of Id-1 constitutively, and Pg showed no effect on Id expression, proliferation, and invasion in these cells. However, after introducing PR (either PR-A or PR-B) into MDA-MB231 cells, Pg inhibited the expression of Id-1 mRNA drastically. PR-transfected MDA-MB231 cells exhibited less proliferative activity after Pg treatment than parental or control MDA-MB231 cells, an effect which correlated well with reduction of Id-1 mRNA. This inhibitory effect on proliferation was accompanied by p21 up-regulation and c-myc down-regulation. Moreover, Pg-treated PR transfectants showed significant morphologic change, appearing more flattened and spread out than control ethanol-treated cells. Boyden chamber invasion assay revealed that PR-transfected MDA-MB231 cells also lost most of their invasive properties after Pg treatment. Zymographic analysis revealed that Pg drastically inhibited matrix metalloproteinase-9 (MMP-9) activity in cells transfected with either PR-A or PR-B. To determine whether Id-1 could act as a key mediator of the effects of Pg, we prepared cells transfected with Id-1 and PR. The morphologic change and p21 up-regulation still were observed after Pg treatment. However, c-myc down-regulation was not observed; the proliferative and invasive activities were mostly recovered; and MMP-9 down-regulation could not be detected anymore. From these observations, we conclude that either form of the PR is sufficient to reduce the malignant phenotypes on treatment with Pg and that Id-1 plays an important role as a mediator of the effects of Pg on breast cancer cell proliferation and invasion.

Role of Id-2 in the maintenance of a differentiated and noninvasive phenotype in breast cancer cells.

Id proteins are inhibitors of basic helix-loop-helix transcription factors and generally stimulate cell proliferation and inhibit differentiation. We have shown that ectopic expression of Id-1 in murine mammary epithelial cells resulted in loss of differentiation and gain of invasive and proliferative abilities. Moreover, Id-1 was highly expressed in aggressive breast cancer cells in culture and in biopsies from infiltrating carcinomas. In contrast to Id-1, we found that, in vitro and in vivo, Id-2 mRNA and protein were up-regulated as mammary epithelial cells lost proliferative capacity and initiated differentiation. We further determined that this up-regulation of Id-2 was a necessary step toward a fully differentiated phenotype in breast cells. Here we show that one of the components of the extracellular matrix network, laminin, is responsible for the increase in Id-2 expression during differentiation. We also show that Id-2 expression is inversely correlated with the rate of proliferation in murine mammary epithelial cells and that Id-2 is expressed at a higher level in differentiated human breast cancer cells in comparison with very aggressive and metastatic cells. When reintroduced in aggressive breast cancer cells, Id-2 is able to reduce their proliferative and invasive phenotypes and decrease their level of matrix metalloproteinase 9 secretion as well as increase syndecan-1 expression. Moreover, little Id-2 protein expression is detectable in human biopsies from aggressive and invasive carcinomas in comparison with in situ carcinomas. In conclusion, Id-2 expression not only follows a pattern opposite to that of Id-1 during mammary gland development and breast cancer progression but also appears to act as an important protein for the maintenance of a differentiated and noninvasive phenotype in normal and transformed breast cells.

Stimulation of the Estrogen Axis Induces Epithelial-Mesenchymal Transition in Human Salivary Cancer cells.

BACKGROUND: Salivary gland cancer is a common type of head and neck cancer characterized by occasional deep invasion and lung metastasis. The precise role of sex steroid hormones in salivary gland cancer is unclear. To address this issue, we investigated whether the estrogen axis modulates salivary adenocarcinoma (SAC) and whether hormone therapy can be an effective treatment. MATERIALS AND METHODS: The estrogen receptor (ER) was overexpressed in HSG human SAC cells that lack endogenous ER and the cells were treated with and without 17ß-estradiol (E2). RESULTS: E2 enhanced malignant phenotypes. Moreover, E2 treatment reduced E-cadherin expression, while increasing that of N-cadherin, vimentin, and inhibitor of differentiation 1 proteins that are associated with the epithelial-mesenchymal transition. Cell invasion was enhanced through activation of matrix metalloproteinase-9. CONCLUSION: These results indicate that hormone therapy used in breast cancer may also be effective for ER-positive SAC.

The Contribution of Dental Implants to Functional Artificial Restoration After Treatment of Oral Cancer.

BACKGROUND/AIM: The aim of this study was to evaluate dental implants with regard to artificial restoration of oral function and quality of life in patients with oral cancer. PATIENTS AND METHODS: We examined 134 implants in 41 patients who had undergone jawbone resection as treatment for oral cancer. The patients were aged 44-89 (mean=61.5) years, and the male to female ratio was 27:14. RESULTS: The 5-year implant success rate was 91.0%. Of the 12 unsuccessful implants, four were embedded on bone grafts with skin flaps, four were embedded on skin flaps using muscle, and four were embedded after peripheral resection. Of the 41 patients, 11 received radiation, but exposure to radiation was not associated with implant loss. The level of satisfaction on the visual analog scale before development of oral cancer was set at 100 mm. Satisfaction fell to 47.0 mm after primary treatment, but recovered to 82.6 mm after implant therapy. CONCLUSION: Patient satisfaction after implant therapy was high, and the implants resulted in improved quality of life. A high proportion of cases involving use of skin flaps resulted in implant loss. Constructing an immobile mucous membrane by replacement of a skin flap with a skin graft may facilitate self-maintenance of implants.

ID1 Controls Aggressiveness of Salivary Gland Cancer Cells via Crosstalk of IGF and AKT Pathways.

BACKGROUND: Inhibitor of differentiation or DNA binding 1 (ID1) is overexpressed in human salivary gland cancer (SGC). The insulin growth factor (IGF) system is an attractive target in cancer control because it is associated with various cancer progressions. MATERIALS AND METHODS: The human SGC cell line HSY with abundant ID1 was used. ID1 knockdown and its effect on the IGF system were investigated. Cell proliferation and invasion, as well as associated protein expression, were analyzed. Phospho-AKT was also evaluated. RESULTS: ID1 knockdown reduced cell proliferation and invasion, while the expression of proteins associated with malignant phenotypes was altered. IGF-II expression was suppressed, suggesting that this system is one of the mechanisms underlying effects of ID1 in SGC cells. c-Myc was up-regulated, whereas p21 and p27 were down-regulated. Moreover, phospho-AKT was reduced in ID1-knockeddown cells. CONCLUSION: ID1 down-regulation induced parallel changes in the IGF and AKT pathways. The crosstalk of these pathways may enhance malignant phenotypes in SGCs.

Introduction of ID2 Enhances Invasiveness in ID2-null Oral Squamous Cell Carcinoma Cells via the SNAIL Axis.

AIM: Inhibitor of DNA-binding (ID) proteins are negative regulators of basic helix-loop-helix transcription factors that generally stimulate cell proliferation and inhibit differentiation. However, the role of ID2 in cancer progression remains ambiguous. Here, we investigated the function of ID2 in ID2-null oral squamous cell carcinoma (OSCC) cells. MATERIALS AND METHODS: We introduced an ID2 cDNA construct into ID2-null OSCC cells and compared them with empty-vector-transfected cells in terms of cell proliferation, invasion, and activity and expression of matrix metalloproteinase (MMP). RESULTS: ID2 introduction resulted in enhanced malignant phenotypes. The ID2-expressing cells showed increased N-cadherin, vimentin, and E-cadherin expression and epithelial-mesenchymal transition. In addition, cell invasion drastically increased with increased expression and activity of MMP2. Immunoprecipitation revealed a direct interaction between ID2 and zinc finger transcription factor, snail family transcriptional repressor 1 (SNAIL1). CONCLUSION: ID2 expression triggered a malignant phenotype, especially of invasive properties, through the ID2-SNAIL axis. Thus, ID2 represents a potential therapeutic target for OSCC.