Role of Autophagy in Acquired Cholesteatoma

Autophagy and its enhancement may have a role in the pathogenesis of acquired cholesteatoma.

The etiopathogenesis of acquired cholesteatoma remains unclear. Some clinical features of cholesteatoma are similar to those of cancer. The study of autophagy in cancer has indicated that enhanced autophagy enables tumor cell survival and growth.

Cholesteatoma epithelium and normal external auditory canal (EAC) epithelium were obtained from patients with acquired cholesteatoma, and marginal epithelium of the tympanic membrane perforation was obtained from patients with chronic otitis media (COM). Immunohistochemistry (IHC) was performed to detect the expression of light chain 3 (LC3) in cholesteatoma and EAC epithelium. Western blotting (WB) was performed to detect the expression of LC3, Beclin-1, or the PI3K/AKT pathway in cholesteatoma, EAC, and COM epithelium.

LC3 staining of IHC was stronger in cholesteatoma epithelium compared with normal EAC epithelium. The ratios of LC3-II/I and Beclin-1 expression on WB were significantly higher in cholesteatoma epithelium compared with EAC epithelium or COM epithelium, and there was a significantly higher ratio of p-PI3K/PI3K and p-AKT/AKT in cholesteatoma epithelium compared with EAC epithelium.

Enhanced autophagy might play a role in the pathogenesis of acquired cholesteatoma. PI3Ks might have different regulatory functions on autophagy in the cholesteatoma epithelium.