25:T51f,Cholesteatoma of the middle ear is a common disease in otolaryngology, which can lead to serious intracranial and extracranial complications. Recent studies showed that the dysregulation of microRNA may be involved in the formation of middle ear cholesteatoma. This study aimed to explore the regulatory effect of micro ribonucleic acid 508-3p (miR-508-3p) on proliferation and apoptosis of middle ear cholesteatoma cells and excavate its underlying regulatory mechanism. We found miR-508-3p expression was upregulated in tissues and cells of cholesteatoma which was inversely related to the expression of hsa_circ_0000007. Overexpression of miR-508-3p could notably facilitate cholesteatoma cell proliferation. Luciferase reporter assay showed that miR-508-3p bound the 3'-untranslated region of its downstream mRNA PTEN. Gain and loss of functions of miR-508-3p were performed to identify their roles in the biological behaviors of cholesteatoma cells, including proliferation and apoptosis. Rescue assays confirmed that PTEN could reverse the effect of miR-508-3p overexpression on cell proliferation. In a word, this study validated that the development of cholesteatoma may regulated by hsa_circ_0000007/miR-508-3p/ PTEN/ PI3K/Akt axis.26:T552,Hearing loss positively links with cigarette smoking. However, the involved mechanism and treatment strategies are largely unrevealed. This study aimed to investigate the damaging effect of nicotine on cochlear hair cells, reveal the underlying mechanism and evaluate the therapeutic effect of melatonin on nicotine-induced injury. The results showed that nicotine induced cytotoxicity of House Ear Institute-Organ of Corti 1 (HEI-OC1) cochlear hair cells in a dose-dependent manner (0, 2.5, 5, 10, 20, 40 and 80 μM). Functional investigations showed that nicotine (10 μM) stimulation dramatically promoted apoptosis, inflammatory response, oxidative stress and endoplasmic reticulum stress in HEI-OC1 cells. Moreover, melatonin treatment dose-dependently alleviated the nicotine-induced cytotoxicity in HEI-OC1 cells (0, 10 25, 50 and 100 μM). Further investigation showed that melatonin (100 μM) effectively attenuated the nicotine-induced apoptosis, inflammation, oxidative stress and endoplasmic reticulum stress in HEI-OC1 cells. Collectively, we demonstrated that nicotine induced apoptosis, inflammation, oxidative stress and endoplasmic reticulum stress of cochlear hair cells in an in vitro cell model. Melatonin showed protective effect on these aspects, suggesting that melatonin may be a potential agent for treating smoking-induced hearing loss.

#	Concept	H-Index	Publications	Citations
1	Medicine	1	1	16
2	Allergy	1	1	16
3	Pharmacology	1	1	16
4	Drug Discovery	1	1	16
5	Drug Resistance	1	1	16

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