Reconstruction of large defects of anterior floor of mouth with free flaps using a novel individualized flap design method.

The purpose of this study was to introduce a novel individualized flap design method for large anterior floor of the mouth (AFOM) defect reconstruction, review experience with the use of this flap design method for large AFOM defect reconstruction, and assess its functional results. A retrospective study of patients who received large AFOM defect reconstruction with free flaps was conducted. There was a cohort of patients who were treated using the novel individualized flap design method and a cohort without flap design. Functional outcomes were evaluated with appropriate scales. Outcomes were analyzed, and a p-value <0.05 was considered significant. 22 patients received the individualized flap design, while 21 patients were treated without a special flap design. All flaps survived. All free flaps harvested with the novel individualized flap design method better matched AFOM defects. Relative to patients without flap design, patients in the novel individualized flap design group showed significant improvement in speech intelligibility (p = 0.036) and swallowing function (p = 0.019). Within the limitation of the study it seems that large AFOM defect reconstruction with the novel individualized flap design method can not only cover and close the wound to avoid oral-neck fistulae, but also maintains tongue mobility to achieve better functional outcomes than in patients without flap design.

A novel flap design technique for subtotal tongue reconstruction with an "Individualized and Convenient Tongue Model".

BACKGROUND: To achieve improved functional outcomes in subtotal tongue reconstruction, a flap design with sufficient volume and appropriate shape is necessary. In this study, we introduce an "Individualized and Convenient Tongue Model" (ICTM) for flap design in subtotal tongue reconstruction. METHODS: By studying the anatomical morphology of the tongue, we found a similar geometry within the dorsum and body of the tongue as well as the mouth floor. This can be used to create an ICTM through folding and splicing. We can simulate tongue defects in the ICTM and transform defect shapes into guide plates for flap design. In this study, fifty-eight patients requiring subtotal tongue reconstruction were randomly divided into two groups: an ICTM group (35 patients) and a conventional group (31 patients). In the ICTM group, we individually designed profunda artery perforator flaps (PAPFs) or anterolateral thigh flaps (ALTFs) using the ICTM method. In the conventional group, the flap was designed according to the surgeon's clinical experience. Patient demographics, operative and follow-up data were recorded. Swallowing, speech intelligibility, and cosmetic results were assessed using appropriate scales. RESULTS: All flaps survived, although there were no significant differences in tumor size, operation time, flap size, and complication rate compared to the conventional group. Patients in the ICTM group had significantly improved speech intelligibility (p = 0.019), cosmetic appearance (p = 0.009), and swallowing ability (p = 0.003). CONCLUSIONS: The ICTM technique is an effective and convenient solution for subtotal tongue reconstruction that provides an individualized flap design and improves functional outcomes compared to the conventional design.

Hsa-let-7e-5p Inhibits the Proliferation and Metastasis of Head and Neck Squamous Cell Carcinoma Cells by Targeting Chemokine Receptor 7.

This study aimed at determining the role of hsa-let-7e-5p in the progression of head and neck squamous cell carcinoma (HNSCC). The relative levels of hsa-let-7e-5p transcripts in 15 paired of HNSCC and adjacent non-tumor tissues and cells were examined by quantitative real-time PCR (qRT-PCR). The potential targets of hsa-let-7e-5p were predicted and validated by luciferase assay. The impact of altered hsa-let-7e-5p expression on HNSCC cell proliferation and metastasis was determined by CCK-8, wound healing, transwell migration and invasion assays. The effect of hsa-let-7e-5p over-expression on the growth of HNSCC was examined in vivo. Hsa-let-7e-5p expression was significantly down-regulated in HNSCC tissues and highly metastatic PCI-37B cells. Bioinformatic analysis predicted that hsa-let-7e-5p bound to the 3'untranslated region (3'UTR) of chemokine receptor 7(CCR7), which was validated by luciferase assay. While transfection with hsa-let-7e-5p mimic significantly decreased CCR7 protein expression, transfection with hsa-let-7e-5p inhibitor increased CCR7 protein expression in HNSCC cells. Similarly, hsa-let-7e-5p over-expression inhibited PCI-37B cell proliferation, wound healing, migration and invasion, while inhibition of endogenous hsa-let-7e-5p had opposite effects in PCI-37A cells. Hsa-let-7e-5p over-expression inhibited PCI-37B tumor growth in vivo. Therefore, hsa-let-7e-5p acts as a tumor suppressor to inhibit the progression of HNSCC by targeting CCR7 expression. Hsa-let-7e-5p and CCR7 may be therapeutic targets of HNSCC.

Overexpression of hsa-miR-125a-5p enhances proliferation, migration and invasion of head and neck squamous cell carcinoma cell lines by upregulating C-C chemokine receptor type 7.

Head and neck squamous cell carcinoma (HNSCC) is usually diagnosed accompanied by lymph node metastasis. C-C chemokine receptor type 7 (CCR7) is associated with the invasion and metastasis of tumors in HNSCC through various signaling pathways. The role of hsa-miR-125a-5p in HNSCC remains unclear. The present study was performed to investigate the association between hsa-miR-125a-5p and CCR7 in HNSCC. Reverse transcription-quantitative polymerase chain reaction was applied to analyze the expression of hsa-miR-125a-5p in clinical samples. Cell Counting Kit-8, Transwell and wound healing assays were used to detect cell proliferation, invasion, and metastasis, respectively, following overexpression of hsa-miR-125a-5p. Changes in protein expression of CCR7 were observed using western blotting. In the survival analysis, Student's t-tests and log rank tests were performed to analyze the association between the expression of hsa-miR-125a-5p, and HNSCC according to the Cancer Genome Atlas database. The expression of hsa-miR-125a-5p was identified to be significantly lower in cancer tissue compared with the corresponding adjacent normal tissues in clinical samples (P=0.038). The results of western blotting indicated that there was a positive regulatory association between hsa-miR-125a-5p and CCR7. Furthermore, overexpression of hsa-miR-125a-5p significantly enhanced the ability of cell proliferation, migration and invasion in HNSCC, with upregulation of CCR7. The results of survival analysis revealed that patients in the low expression group of hsa-miR-125a-5p tended to have longer survival times compared with the high expression group (P=0.045). Altogether, the data raised the possibility that hsa-miR-125a-5p has a significant role in promoting cancer in HNSCC, which may provide a basis for the treatment of HNSCC in molecular targeted therapy. Further studies are required to ascertain the role of hsa-miR-125a-5p in other HNSCC cell lines and in vivo.

Upregulated miR­20a­5p expression promotes proliferation and invasion of head and neck squamous cell carcinoma cells by targeting of TNFRSF21.

MicroRNAs (miRNAs) play important roles in regulation of proliferation, migration, and invasion of head and neck squamous cell carcinoma (HNSCC). The present study assessed expression, functions and mechanisms of miR­20a­5p in the regulation of HNSCC cell proliferation, migration and invasion. miR­20a­5p expression in HNSCC cell lines and tissues was detected using qRT­PCR, while miR­20a­5p mimics and inhibitor were transfected into HNSCC cells for assessment of the effects using different assays (CCK­8, wound healing and Transwell assays) and expression of miR­20a­5p­targeting genes (using western blot and luciferase reporter assays). The data revealed that miR­20a­5p was upregulated in both HNSCC tissues and metastatic HNSCC cells. Upregulated miR­20a­5p expression in HNSCC cells promoted tumor cell proliferation, migration and invasion capacities, but resulted in downregulation of TNFRSF21 expression and in turn upregulation of C­C motif chemokine receptor 7 (CCR7) in HNSCC cells. Concordantly, knockdown of miR­20a­5p in HNSCC had the opposite results. In conclusion, miR­20a­5p functioned as an oncogene in HNSCC by downregulating TNFRSF21 and subsequently, upregulating CCR7 expression.

MiR-1275 promotes cell migration, invasion and proliferation in squamous cell carcinoma of head and neck via up-regulating IGF-1R and CCR7.

PURPOSE: miRNAs can play vital role in migration, invasion and proliferation in Squamous cell carcinoma of head and neck (SCCHN). In our study, we attempted to validate the expression and function of miR-1275 in SCCHN, and we also identified the mechanism by which miR-1275 affects migration, invasion and proliferation of SCCHN. METHODS: Real-time polymerase chain reaction (RT-PCR) was employed to evaluate the expression of miR-1275 in both SCCHN tissues and cell lines. The role of miR-1275 in SCCHN cells was verified by cell function experiments upon transfection with miR-1275 mimics and inhibitor. Western blot analysis was employed to test the target gene expression of miR-1275. Survival analysis was made with the information of SCCHN patients expressed miR-1275 from The Cancer Genome Atlas (TCGA) database. RESULTS: miR-1275 expression was up-regulated in SCCHN tissues and advanced metastatic SCCHN cells. Increasing miR-1275 expression in SCCHN could promote cell migration, invasion and proliferation probably by upregulating Insulin-like growth factor 1 receptor (IGF-1R) and C-C chemokine receptor type 7(CCR7) protein levels, whereas inhibition of miR-1275 could lead the opposite effects, although others have already demonstrated that IGF-1R is a direct target of miR-1275. Survival analysis suggested that patients with lower miR-1275 expression may have a better outcome. CONCLUSIONS: Herein we report for the first time that miR-1275 could act as a tumor-promoter in SCCHN possibly by regulating its target gene via novel miRNA mechanisms. MiR-1275 plays an important role in promoting SCCHN progression. The miR-1275 may be a potential therapeutic target for SCCHN treatment in the future.