Objective To investigate clinic value of real-time shear wave elastography (SWE) in indentifying benign salivary gland mass through measuring tissue elastic properties of the benign mass in salivary gland.Methods Seventy-four patients with benign salivary gland mass were enrolled.All of them have been obtained the average elasticity modulus of the mass by SWE before surgery,including parotid mixed tumor (22),parotid adenolymphoma (13) and sub maxillary gland mixed tumor (6),adenolymphoma (33).Statistical analysis was done between groups.Results The average elasticity modulus in parotid mixed tumor group and sub maxillary gland mixed tumor group exhibited (133.53 ± 3.35)kPa and (125.57 ± 2.89)kPa respectively.The average elasticity modulus in parotid aden lymphoma group and sub maxillary gland adenolymphoma group exhibited (65.60 ± 2.33)kPa and (64.60 ± 1.93)kPa respectively.There was no significant difference between mixed tumor group and there was no significant difference between adenolymphoma group.There were significant differences between mixed tumor group and adenolymphoma group.ConcLusions The SWE can distinguish salivary gland benign mass from different originates,which can provide more evidence for clinical diagnosis.

Objective: To investigate the role of transcription factor specificity protein 1 (SP1) in proliferation, migration and invasion in head and neck squamous cell carcinoma (HNSCC), and the role of SP1 in transcription regulation of microRNA (miRNA)-92b. Methods: Predicted the possible target miRNA of transcription factor SP1 by bioinformatic analysis. Furthermore, confirmed the binding sites of transcription factor SP1 and miRNA-92b promoter regions by chromatin immunoprecipitation. After transfecting SP1 siRNA and negative control siRNA, also performed quantitative real-time PCR (qPCR), cell proliferation assay and Transwell assay. Results: The bioinformatic analysis shows SP1 is a possible transcription factor of miRNA-92b. Chromatin immunoprecipitation suggests there are three binding sites in miRNA-92b promoter regions that can be combined with SP1. qPCR suggests in PCI-4A and PCI-37A cells the expression of SP1 in experimental group (respectively was 0.064±0.020 and 0.639±0.008) were significantly lower than negative control group (both were 1)(P<0.05). In PCI-4A and PCI-37A cells the expression of miRNA-92b in experimental group (respectively was 0.215±0.033 and 0.497±0.104) were significantly lower than negative control group (both were 1)(P<0.05). In experimental group proliferation of SP1 in PCI-4A and PCI-37A cells value A were significantly lower than negative control group (P<0.05). In experimental group migration of SP1 in PCI-4A and PCI-37A cells (respectively was 37.0±4.6 and 40.7±2.1) were significantly lower than negative control group (101.0±5.3 and 82.7±5.7) (P<0.05). In experimental group invasion of SP1 in PCI-4A and PCI-37A cells (respectively was 31.3±10.8 and 37.0±4.6) were significantly lower than negative control group (92.3±3.1 and 70.3±3.1)(P<0.05). Conclusions SP1 promotes proliferation, migration and invasion abilities of HNSCC cells. SP1 is a transcription factor of miRNA-92b and can directly be involved in transcription regulation of miRNA-92b.