The plasma levels of miR-24-3p, miR-16-5p, miR-185-5p, and miR-451a were upregulated during noise exposures, and increased levels of miR-21 have been found in vestibular schwannomas and human cholesteatoma.
Considering the function of miR‑21 in the regulation of proliferation and apoptosis, let‑7a may control cell proliferation and apoptosis by regulating miR‑21, and its targets, in cholesteatoma keratinocytes.
The levels of TLR-2, -3, -4, -6, -7, and -10, NOD-2, and IL-1 and -8 mRNAs were significantly higher in the cholesteatoma than in the skin specimens (p < .05).
It is possible that upregulation of miR-21 leads to higher tumour cell proliferation and invasion of cholesteatoma in children than adults, and the benign nature of cholesteatoma may be due to a balance between let-7a microRNA and miR-21.
Proposed upstream regulators of hsa-miR-21 expression (CD14, interleukin 6R, gp130, and signal transducer and activator of transcription 3) were present in all cholesteatoma tissues.
We suggest that both of IL-1 alpha and IL-1 beta may play a role in the pathological changes, and that IL-8, which is mainly produced from cholesteatomatous epithelium, may have an important role in the pathological changes of cholesteatomas.
The concentrations of four candidate factors, namely interleukin-1β, interleukin-6, tumor necrosis factor α, and prostaglandin E2, were increased in cholesteatomas compared with normal skin.
Positive HB-EGF immunostaining observed in the basal and suprabasal layers of cholesteatoma epithelium was significantly stronger than in normal postauricular skin.
This study suggested that persistent expression of extracellular HMGB-1 and DNA fragments in cholesteatoma leads to TNF-α and IL-1β production, causing bone resorption and destruction.
The significant difference in c-MYC gene expression level in cholesteatoma compared to that of atheroma implies a more prominent hyperproliferative phenotype which may explain the clinical behavior typical of cholesteatoma.
The levels of TLR-2, -3, -4, -6, -7, and -10, NOD-2, and IL-1 and -8 mRNAs were significantly higher in the cholesteatoma than in the skin specimens (p < .05).
A previous study has reported that the expression of KGF receptor is increased in more differentiated areas of the cholesteatoma tissue, whereas the expression of the epidermal growth factor receptor is associated with proliferative and migratory areas of the lesion.
These findings suggest that the ability of hyperproliferation of primary acquired cholesteatoma might have been related to c-MYC copy number by deregulating c-MYC expression.
We suggest that both of IL-1 alpha and IL-1 beta may play a role in the pathological changes, and that IL-8, which is mainly produced from cholesteatomatous epithelium, may have an important role in the pathological changes of cholesteatomas.
Expression of c-myc was studied in cholesteatoma epithelium using a monoclonal antibody directed against the 67 kDa c-myc protein product and the alkaline phosphatase-antialkaline phosphatase method.
The signal of the EGF mRNA was slightly expressed in part of the basal cells in only one of the six control specimens, while the signal was strongly expressed along the basal cells of the cholesteatoma epithelium in five of the ten specimens.