Background: The major histocompatibility complex class I chain-related molecule A (MICA) is one of the natural killer group 2D ligands. Soluble major histocompatibility complex class I chain-related molecule A (sMICA) mediates tumor immune escape, but the mechanism is not fully understood. In this study, we examined the expression of phospho-p38, matrix metalloproteinase 9 (MMP-9), and MICA and their relationships among each other in pituitary adenoma tissues to provide a histologic basis for the mechanism of pituitary adenoma immune escape.

Methods: We applied immunohistochemistry, real-time quantitative reverse-transcriptase polymerase chain reaction, and Western blot to detect phospho-p38, MMP-9, and MICA expression at the mRNA and protein levels in pituitary adenoma tissues. Enzyme-linked immunosorbent assay was used to examine the expression levels of MMP-9 and sMICA in peripheral blood serum from patients with pituitary adenoma.

Results: We found that p38, MICA, and MMP-9 mRNA levels were greater in pituitary adenomas than in normal tissues. The phospho-p38, MMP-9, and MICA proteins were overexpressed in pituitary adenomas, and the expression of MMP-9 and MICA were positively correlated with the expression of phospho-p38. In addition, the serum levels of sMICA and MMP-9 proteins in pituitary adenoma patients were significantly greater than those in normal controls.

Conclusions: These findings suggest that activation of the p38/mitogen-activated protein kinase pathway may increase MICA expression and induce MMP-9 expression. MMP-9 is involved in the shedding of sMICA from MICA to promote tumor immune escape. Furthermore, p38/mitogen-activated protein kinase could potentially represent a novel target for inhibiting pituitary adenoma immune escape.

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http://dx.doi.org/10.1016/j.wneu.2018.11.077DOI Listing

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