miR-183/TMSB4Y, a new potential signaling axis, involving in the progression of laryngeal cancer via modulating cell adhesion.

Laryngeal cancer (LCa) is a prevalent malignant head and neck cancer with relatively unclear pathogenesis. A prior study has suggested that miR-183 differentially expressed in laryngeal-related malignancies, but its accurate role has not been fully ascertained in LCa. miR-183 expression in LCa tissues and cells was detected assisted by TCGA/GEO databases or qRT-PCR assay, relatively. Target genes of miR-183 were predicted via accessing to TargetScan website. Luciferase activity analysis was conducted to determine the relationship between miR-183 and its possible target. CCK-8, colony formation and transwell invasion and migration experiments were implemented to measure LCa cell viability, invasion and migration. Western blot assay was utilized to evaluate cell adhesion and EMT-related proteins expressions. The expression of miR-183 was expressed in LCa tissue samples and cells at higher levels than normal controls. Upregulation of miR-183 facilitated Hep-2 and TU212 cells viability, while miR-183 reduction inhibited the proliferative potential of Hep-2 and TU212 cells. TMSB4Y was determined as a possible target of miR-183, and its expression was decreased in LCa. LCa patients with low TMSB4Y expression had poorer outcomes relative to that with high TMSB4Y expression. TMSB4Y overturned the promoting impacts of miR-183 on the LCa cellular malignant behaviors, including cell proliferation, colonogenicity, invasion and migration. miR-183 overexpression inhibited cell adhesion through inhibiting TMSB4Y expression. Overall, all results elucidated that miR-183, as an oncogenic molecule in LCa, may be used to predict the prognosis of LCa patients by targeting TMSB4Y.

[Effects of sodium salicylate on the expressions of gamma-aminobutyricacid and glutamate and auditory response properties of the inferior colliculus neurons].

The effects of sodium salicylate (NaSA) on the expressions of gamma-aminobutyricacid (GABA) and glutamate (Glu), and auditory response properties of the inferior colliculus neurons in mice were studied. Thirty-six Kunming mice were divided into three groups: control group (saline injection); NaSA group (NaSA 450 mg/kg, i.p., each day for 15 d); NaSA + lidocaine group (NaSA 450 mg/kg + lidocaine 10 mg/kg, i.p., each day for 15 d). The expressions of GABA and Glu were examined with immunohistochemical method. The intensity-rate function, intensity-latency function and frequency-tuning curve were determined with extracellular electrophysiological recording. Results are as follows: (1) The expression of GABA in the NaSA and NaSA + lidocaine groups decreased remarkably compared with that in the control group; there was no noticeable difference between the NaSA and NaSA + lidocaine groups. The expression of Glu in the NaSA group increased significantly compared with that in the control and NaSA + lidocaine groups. No difference in the expression of Glu was found between the control and NaSA + lidocaine groups. (2) In NaSA group, the intensity-rate function displayed a non-monotonic pattern, rising at low intensity and descending at high intensity; the tip of frequency-tuning curves became broad after administration of NaSA. (3) The changes in intensity-rate function and intensity-latency function were not evident and the tips of the frequency-tuning curves sharpened in the NaSA + lidocaine group. These results suggest that administration of NaSA increases the expression of Glu-positive neurons and reduces that of GABA-positive neurons in the inferior colliculus. NaSA changes the auditory response properties of the inferior colliculus and lidocaine can reverse these changes.