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Objective: The aim of this study was to investigate the effect of mammalian‐enabled (Mena) on tongue squamous cell carcinoma (TSCC) metastasis and its mechanism. Materials and Methods: Immunochemistry was performed to investigate the Mena and tumor‐related markers expression, and its clinicopathological characteristics in 46 TSCC specimens. TSCC cell SCC9 and Cal27 untransfected or stable transfected with Mena overexpression and small interfering RNA were used to determine the role of Mena in cell proliferation, cell migration, invasion and metastasis, and EMT‐related markers in vitro, and the effect of Mena on TSCC growth and metastasis through tumor‐bearing and tumor metastasis immunodeficient mice models in vivo. Results: Immunochemistry showed that the expression of Mena was significantly correlated with lymphatic metastasis and TNM stage, E‐cadherin, Vimentin, and MMP2. Mena did not affect cell proliferation and colony formation in vitro, and tumor growth in vivo. However, it promoted cell migration and invasion in vitro, and TSCC metastasis in vivo. Conclusions: Mena expression is associated with lymphatic metastasis and tumor stage and promotes TSCC invasion and metastasis by inducing the EMT process. Thus, Mena may be a biomarker for prognosis and targeted therapy in TSCC patients. [ABSTRACT FROM AUTHOR]

Objective: The effect of miR-626 on the radiosensitivity to oral squamous cell carcinoma (OSCC) was evaluated in this study. Materials and Methods: The level of miR-626 in OSCC patients was determined by analyzing the data of miRNA microarray GSE113956. miR-626 was overexpressed by miR-626 mimics and knockdown were performed by miR-626 inhibitor. The level of miR-626 was detected by quantitative real-time polymerase chain reaction. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony formation assays were used to detect the effect of miR-626 on the growth of OSCC cells. Flow cytometry was used to detect the apoptosis of OSCC cells. Western blot and dual luciferase reporter assays were used to explore the underlying mechanism of miR-626 regulating the radiosensitivity to OSCC. The effect of miR-626 on the radiosensitivity to OSCC were examined in an in vivo xenograft model. Results: The serum miR-626 level of OSCC patients was significantly higher than that of healthy controls. miR-626 mimics significantly promoted the OSCC cell growth, but the miR-626 inhibitor significantly suppressed the OSCC cell growth. Radiation combined with the miR-626 inhibitor significantly suppressed the cell proliferation and promoted the apoptosis of SCC-4 and HSC4 cells. Moreover, miR-626 regulates the nuclear factor kappa-B (NF-κB) signaling mediated by TRAF-interacting protein with forkhead-associated domain B. Furthermore, inhibition of miR-626 enhances the radiosensitivity to OSCC in nude mice. Conclusions: miR-626 inhibition enhanced the radiosensitivity to OSCC through the downregulation of NF-κB signaling. [ABSTRACT FROM AUTHOR]

Increasing evidence has shown that aberrant miRNAs contribute to the development and progression of human melanoma. Previous studies have shown that miR-125b functions as a suppressor in malignant melanoma. However, the molecular function and mechanism by which miR-125b influences melanoma growth and invasion are still unclear. In this study, we aimed to investigate the role of miR-125b in melanoma progression and metastasis. We found that miR-125b expression is significantly downregulated in primary melanoma, and an even greater downregulation was observed in metastatic invasion. Restored expression of miR-125b in melanoma suppressed cell proliferation and invasion both in vitro and in vivo. Furthermore, our findings demonstrate that upregulating miR-125b significantly inhibits malignant phenotypes by repressing the expression of integrin alpha9 (ITGA9). Finally, our data reveal that upregulated expression of ITGA9 in melanoma tissues is inversely associated with miR-125b levels. Together, our results demonstrate that upregulation of ITGA9 in response to the decrease in miR-125b in metastatic melanoma is responsible for melanoma tumor cell migration and invasion. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the usefulness of the modified cosmetic incision (MCI) and advanced wound closure method in partial parotidectomy by comparison with the modified Blair incision (MBI).Patients and Methods: This study retrospectively enrolled 44 patients who underwent partial parotidectomy for benign parotid tumors. These patients were divided into 2 groups: MCI group and MBI group. The MCI surgical procedures were performed via a minimal facelift incision with no preauricular incision, postauricular and hairline incision, or extensive hairline incision and an advanced wound closure method, using continuous absorbable intradermal sutures and skin adhesive. The MBI surgical procedures were performed via a conventional MBI and standard transdermal, interrupted, nonabsorbable suturing approach. The operation variables and the cosmetic results of the patients in each group were compared.Results: A total of 23 patients underwent the MCI and advanced wound closure approach and 21 patients underwent the MBI and standard wound closure approach. No significant differences were found in gender, mean age, tumor size, or tumor site between the 2 groups (P > .05). No differences between groups were seen in operative time and intraoperative blood loss volume (P > .05). Several postoperative complications, such as facial paralysis, Frey syndrome, salivary fistula, infection, or tumor recurrence, did not differ between the 2 groups (P > .05). However, postoperative drainage volume in the MCI group was significantly lower than that in the MBI group (P < .01). Moreover, the postoperative cosmetic satisfaction, skin numbness, and scar evaluation results in the MCI group were better than those in the MBI group (P < .001).Conclusions: MCI combined with continuous absorbable intradermal sutures and skin adhesive for partial parotidectomy is technically feasible and safe and could produce excellent cosmetic outcomes in selected patients with benign parotid tumors. [ABSTRACT FROM AUTHOR]

Increasing evidence has shown that aberrant miRNAs contribute to the development and progression of human melanoma. Previous studies have shown that miR-125b functions as a suppressor in malignant melanoma. However, the molecular function and mechanism by which miR-125b influences melanoma growth and invasion are still unclear. In this study, we aimed to investigate the role of miR-125b in melanoma progression and metastasis. We found that miR-125b expression is significantly downregulated in primary melanoma, and an even greater downregulation was observed in metastatic invasion. Restored expression of miR-125b in melanoma suppressed cell proliferation and invasion both in vitro and in vivo. Furthermore, our findings demonstrate that upregulating miR-125b significantly inhibits malignant phenotypes by repressing the expression of integrin alpha9 (ITGA9). Finally, our data reveal that upregulated expression of ITGA9 in melanoma tissues is inversely associated with miR-125b levels. Together, our results demonstrate that upregulation of ITGA9 in response to the decrease in miR-125b in metastatic melanoma is responsible for melanoma tumor cell migration and invasion.