[Application of intraoral ultrasonic imaging in diagnosis and treatment of 18 patients with oral leukoplakia in non-masticatory mucosa].

PURPOSE: To explore the sonographic appearance of leukoplakia in non-masticatory oral mucosa, classifying mucosal leukoplakia according to the characteristics of sonogram, and providing reference for clinical diagnosis and treatment. METHODS: Eighteen patients (24 lesions) were diagnosed as oral leukoplakia at the Department of Oral Mucosal Diseases, Shanghai Ninth People's Hospital. The lesions were located in the tongue, floor of mouth, buccal mucosa and libial mucosa. Before the biopsy was taken, intra-oral path ultrasound was performed at the Department of Ultrasound to observe the lesion's extent, continuity, presence or absence of keratinization, the thickness of each layer in the epithelium, and color doppler flow imaging of the lesions. Quantitative analysis software 'Qontraxt' was used to randomly measure the relative echo intensity of the mucosal surface in leukoplakia areas, and summarize the keratinization type. SPSS 25.0 software package was used for statistical analysis of the data, and paired t test was used for inter-group comparison of the data. RESULTS: Oral leukoplakia sonograms showed that the epithelial layer appeared keratinization, the epithelial was thickened, and the echo was enhanced. The stratum intermedium showed a low echo thickening band, and the echo of partial lesions' surface decreased or the blood flow signal in oral mucosa increased. The hyperechoic band in the leukoplakia area was significantly thickened (P<0.001), and the echo was enhanced, with the tongue and buccal mucosa being the most significant. The hypoechoic band was significantly thicker (P<0.001), with the buccal mucosa and labial mucosa being the most significant. The surface and stratum corneum echo intensity values were determined by Qontraxt quantitative analysis software to determine whether there were keratinization and the keratinization types. The echo intensity values was 43.28±9.33 in non-OLK area, 92.88±3.12 in OLK with orthokeratosis, and 84.75±5.76 in OLK with parakeratosis. CONCLUSIONS: Ultrasound imaging can effectively define mucosal leukoplakia and measure the thickness of each layer in the epithelium. In addition, special adjoint changes such as ulcers, infections and cancerous changes can be detected. Intraoral ultrasonic imaging can provide imaging evidence for clinical diagnosis, treatment planning and post-treatment follow-up and contribute to avoid unnecessary mucosal iatrogenic injury or recurrence of disease after treatment.

Retracted: Long noncoding RNA MEG3 inhibits proliferation and migration but induces autophagy by regulation of Sirt7 and PI3K/AKT/mTOR pathway in glioma cells.

Glioma is a common primary brain tumor with high mortality rate and poor prognosis. Long noncoding RNA maternally expressed gene 3 (MEG3) is a tumor suppressor in diverse cancer types. However, the role of MEG3 in glioma remains unclear. We aimed to explore the effects of MEG3 on U251 cells as well as the underlying mechanisms. U251 cells were stably transfected with different recombined plasmids to overexpress or silence MEG3. Effects of aberrantly expressed MEG3 on cell viability, migration, apoptosis, expressions of apoptosis-associated and autophagy-associated proteins, and phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all evaluated. Then, messenger RNA (mRNA) and protein expression of Sirt7 in cells abnormally expressing MEG3 were estimated. In addition, effects of abnormally expressed MEG3 and Sirt7 on U251 cells were determined to reveal the underlying mechanism of MEG3-associated modulation. Cell viability and migration were significantly reduced by MEG3 overexpression whereas cell apoptosis as well as Bax and cleaved caspase-3/-9 proteins were obviously induced. Beclin-1 and LC3-II/LC3-I were upregulated and p62 was downregulated in MEG3 overexpressed cells. In addition, the autophagy pharmacological inhibitor (3-methyladenine, 3-MA) affected the effect of MEG3 overexpression on cell proliferation. Furthermore, the phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all reduced by MEG3 overexpression. Sirt7 was positively regulated by MEG3 expression, and effects of MEG3 overexpression on U251 cells were ameliorated by Sirt7 silence. MEG3 suppressed cell proliferation and migration but promoted autophagy in U251 cells through positively regulating Sirt7, involving in the inhibition of the PI3K/AKT/mTOR pathway.