Application of Crus of Helix Incision Through the Posterior Parotid Gland Approach in the Mid-Level or High-Level Mandibular Condylar Fractures.

OBJECTIVE: This study is to explore the clinical effect of crus of helix incision through the posterior parotid gland approach in the treatment of Mid-or High-Level mandibular condylar fractures. METHODS: From September 2020 to June 2023, we performed incision reduction internal fixation of 23 patients with mid-level or high-level fractures of the mandibular condylar through the approach of the posterior parotid gland, and observed the effect of the operation. RESULTS: After a follow-up period of 6 to 12 months, all patients showed no signs of postoperative facial paralysis or salivary gland fistula. In addition, satisfactory scars were observed in the operation area, and the occlusion function had recovered well. CONCLUSION: The approach of using a crus of helix incision through the posterior parotid gland proved to be an effective method for treating mid-level or high-level fractures of the condylar fractures. This technique offers several advantages, including adequate exposure, minimal facial nerve injury, ease of incision and reduction, inconspicuous scarring, and a more concealed incision.

lncRNA TSPEAR-AS2, a Novel Prognostic Biomarker, Promotes Oral Squamous Cell Carcinoma Progression by Upregulating PPM1A via Sponging miR-487a-3p.

BACKGROUND: Long noncoding RNA (lncRNA) critically impacts the modulation of tumor developments and progressions. Our study is aimed at investigating the expressing patterns, clinical significance, and biological roles of lncRNA TSPEAR-AS2 (TSPEAR-AS2) in oral squamous cell carcinoma (OSCC). Material and Approach. The expressing states achieved by TSPEAR-AS2 were examined in OSCC specimens and cell lines by RT-PCR. The clinical significance of TSPEAR-AS2 was statistically analyzed. OSCC proliferating, invading, and migrating processes were examined with the use of wound healing assays, transwell, colony formation, and cell counting kit-8. Additionally, the downstream molecular mechanism of TSPEAR-AS2 in OSCC was explored. RESULTS: TSPEAR-AS2 was overexpressed in OSCC tumors and cells. High TSPEAR-AS2 was associated with advanced TNM stage. Patients with high TSPEAR-AS2 expression displayed a shorter disease-free survival and total survival of OSCC patients than those with low TSPEAR-AS2 expressing level. It was found that knockdown of TSPEAR-AS2 could inhibit the proliferating, invading, and migrating processes pertaining to OSCC cells. Luciferase reporter tests and RNA pull-down results revealed that TSPEAR-AS2 enhanced the expressions of PPM1A by regulating miR-487a-3p, and TSPEAR-AS2 could be adopted as a miR-487a-3p sponge to inhibit PPM1A expression. CONCLUSION: Our study highlighted the significance of the TSPEAR-AS2/miR-487a-3p/PPM1A axis within OSCC progression and offered a novel biomarker and novel strategies for OSCC treatments.

Expression of tumor-associated calcium signal transducer 2 in patients with salivary adenoid cystic carcinoma: Correlation with clinicopathological features and prognosis.

Salivary adenoid cystic carcinoma (SACC) is a common salivary malignancy. The current treatment option for SACC is complete surgical excision with postoperative radiotherapy. The prognosis remains unsatisfactory, due to frequent local recurrence and distant metastases that directly reduce the overall survival time. Previous studies have shown that overexpression of tumor-associated calcium signal transducer 2 (TACSTD2) is associated with poor prognosis in various human epithelial cancers. The expression of TACSTD2 in SACC is currently unknown. The present study therefore aimed to retrospectively investigate TACSTD2 protein expression by immunohistochemistry on paraffin-embedded primary tumor tissue samples from a series of consecutive SACC patients (n=81). The correlation of TACSTD2 expression with clinicopathological variables was evaluated using either the Kruskal-Wallis or Mann-Whitney statistical tests. The survival curves were plotted using the Kaplan-Meier method. The parameters of prognostic significance found by univariate analysis were verified in a multivariate Cox regression model. Overexpression of TACSTD2 was detected in 35/81 (44%) SACC patients and was significantly associated with a decreased overall survival (P<0.01). Univariate analysis showed that TACSTD2 overexpression was correlated with TNM stage (P=0.020), local recurrence (P=0.002) and distant metastasis (P=0.001). Multivariate analyses further revealed that TACSTD2 may be an independent prognostic indicator. In conclusion, TACTSD2 could be recognized as an independent prognostic indicator for SACC. Gene therapy targeting TACSTD2 may be a possible treatment approach for patients with SACC overexpressing this cell-surface marker.

[Differential proteomics research on exosomes derived from tongue squamous cell carcinoma cells and normal mucosa cells].

OBJECTIVE: This study aimed to explore further the mechanisms of tongue squamous cell carcinoma (TSCC) cell recurrence, metastasis, and diffusion, as well as to establish the experimental basis for the molecular biology research on TSSC. We intend to complete our objective through differential proteomics and preliminary analysis protein expression of exosomes derived from TSCC and normal mucosa cells. METHODS: We acquired cultured supernatant fluid in vitro in the laboratory by culturing TSCC (tongue cancer Tca8113 cell line) and human normal mucosa cells (HOK cell line). The exosomes were separated and purified through differential centrifugation. Furthermore, the different protein expressions were identified through dielectrophoresis and mass spectrometry. The functions of the different protein expressions were identified through an online database search. RESULTS: TSCC and human normal mucosa cells secrete a large amount of capsule bubble structure substances in vitro, as confirmed by electron microscopy and surface markers heat shock protein-70 and major histocompatibility complex class 1. A total of 16 oral cancer cell-derived exosomes that expressed quantity more than two times, twelve that increased their expression levels, and four that cut their expressions were identified through the differential proteomics research on the two groups. CONCLUSION: Differential proteins that were verified through the online database serve an important function in exosome formation and in the progress of cancer.

[The molecular mechanism between interstitial fluid pressure and malignant phenotype of salivary adenoid cystic carcinoma].

OBJECTIVE: To explore the effects of stress imposed on adenoid cystic carcinoma (ACC), therefore to clarify the molecular basis and mechanism of ACC's malignant phenotype under the elevated tumor interstitial fluid pressure. METHODS: ACC cells were cultured under pressure (103.74 kPa), and were divided into four groups (3 h group, 6 h group, 12 h group, 24 h group) according the pressure time. Untreated ACC2 was as negative control group, untreated ACCM was as positive control group. The level of epidermal growth factor receptor (EGFR) was detected by semiquantitative analysis of immunochemistry. Matrix metalloproteinase 9 (MMP9) and EGFR mRNA expression were assessed by reverse transcriptase polymerase chain reaction. EGFR, phosphorylation epidermal growth factor receptor (P-EGFR), MMP9, keratinocyte growth factor (KGF) and phosphorylation extracellular signal-regulated kinase (P-ERK) protein expressions were assessed by Western blot. RESULTS: As the extension of pressure time, the expression of EGFR, P-EGFR, MMP9, KGF, P-ERK in ACC2 gradually increased, which were positive correlation with pressure time, and were higher than that of negative control group. CONCLUSION: Under the stimulation of pressure, the mRNA and protein levels of adhesion molecules and metastatic relative molecules in ACC2 were sharply elevated.

Induction of ER stress-mediated apoptosis by ceramide via disruption of ER Ca(2+) homeostasis in human adenoid cystic carcinoma cells.

BACKGROUND: Ceramides are a class of sphingolipids that form the structural component of the cell membrane and also act as second messengers in cell signaling pathways. Emerging results suggest that ceramide induces growth arrest and apoptosis in various human cancer cells. However, the mechanisms underlying its antitumor activity are yet to be identified. Endoplasmic reticulum stress (ER stress), a cellular adaptive response, is believed to initially compensate for damage but can eventually trigger cell death if the stimulus is severe or prolonged. In this study, we investigated whether ceramide induces cell death in human salivary adenoid cystic carcinoma (ACCs) through activation of the apoptotic ER stress. RESULTS: RT-PCR, real-time PCR and western blot demonstrated that exogenous ceramide treatment up-regulated GRP78 and p-eIF2α expression and XBP1 splicing. Moreover, the ceramide synthase inhibitor FB1 abolished ceramide-induced ER stress. Up-regulation of the ER stress-associated apoptosis promoting transcription factor CHOP and p-JNK suggested that the antitumor activity of ceramide is owing to activation of apoptotic ER stress. Mechanistically, [Ca(2+)]ER depletion and SERCA inhibition by ceramide treatment suggested that it induces ER stress by disrupting [Ca(2+)]ER homeostasis. The chemical chaperone TUDCA inhibited ceramide-induced ER stress and cell death. In addition, the downstream metabolite of ceramide, S1P, cannot activate ER stress. CONCLUSIONS: These results demonstrated that exogenous ceramide induces cancer cell death through a mechanism involving severe ER stress triggered by the disruption of ER Ca(2+) homeostasis.

EGFR inhibition prevents in vitro tumor growth of salivary adenoid cystic carcinoma.

BACKGROUND: Epidermal growth factor receptor (EGFR) is involved in the development of many human malignant tumors and plays an important role in tumor growth and metastasis. Antagonists of EGFR can suppress the growth of several malignancies; however, their therapeutic effect in adenoid cystic carcinoma (ACC) is controversial. RESULTS: The increased proliferation of two ACC cell lines induced by EGF-treatment was reversed by nimotuzumab. Regardless of EGF stimulation, nimotuzumab-treated ACC cells were arrested in G1 phase and showed decreased expression of Ki67. In addition, EGF activated the MAPK-dependent pathway and up-regulated the expression of matrix metalloproteinase-9 and Snail, enhancing the invasive potential of an ACC cell line (ACC-M). The effects of EGF were down-regulated by nimotuzumab treatment. CONCLUSIONS: These results suggest that nimotuzumab can inhibit the growth and invasion of ACC cells induced by EGF, probably through inactivation of ERK phosphorylation. Thus, nimotuzumab should be considered as a promising novel agent for the treatment of ACC.

Cancer stem cell-like cells exist in mucoepidermoid carcinoma cell line MC3.

Strong evidence for the presence of cancer stem cells (CSCs) in tumors exists. CSCs play an important role in the development, invasion, and drug resistance of carcinoma. Poorly differentiated mucoepidermoid carcinoma (MEC) is a lethal malignancy of human salivary gland tumors. However, whether there are CSCs in MEC and their phenotypes remains unclear. We isolated side population (SP) and sphere-forming cells from the MEC cell line MC3 and identified their characteristics. The results showed that sphere-forming assays could enrich stem cell-like cells, with this group of cells exhibiting high cloning efficiency, possessing strong tumorigenic ability, and highly expressing Oct4 based on PCR and immunocytochemistry assays. They also highly expressed CD44 and lowly expressed CD24 according to PCR, immunocytochemistry assays, and fluorescence-activated cell sorting analysis. Higher cloning efficiency was observed in the SP cells, but PCR revealed that the SP and non-SP cells did not statistically differ in their expression of ABCG2, Oct4, CD44, and CD24. In spite of these, the findings were not conclusive on whether SP cells are stem cell-like cells. In conclusion, CSC-like cells do exist in the MC3 cell line, and sphere-forming assays could enrich them, sphere-forming and SP cells are not the same kind of cell subpopulations, and the characteristics of SP cells need to be further investigated.