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2017 ; 15
(6
): 4123-4131
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Interleukin?6 induces an epithelial?mesenchymal transition phenotype in human
adamantinomatous craniopharyngioma cells and promotes tumor cell migration
#MMPMID28487953
Zhou J
; Zhang C
; Pan J
; Chen L
; Qi ST
Mol Med Rep
2017[Jun]; 15
(6
): 4123-4131
PMID28487953
show ga
Total resection of adamantinomatous craniopharyngioma (ACP) is complex and often
leads to postoperative recurrence. This is due to the tendency of the tumor to
invade the surrounding brain tissue and the generation of a local inflammatory
state between the tumor cells and parenchyma. While there is evidence to suggest
that interleukin?6 (IL?6) induces craniopharyngioma (CP)?associated inflammation,
particularly in ACP, the role of IL?6 in the progression of ACP remains unclear.
The results of the present study demonstrated that CP inflammation was associated
with pathological classification, extent of surgery, degree of calcification and
postoperative hypothalamic status scale. Cytokine antibody arrays were conducted
to measure the expression of IL?6 and other inflammatory factors in tumor tissues
in response to various levels of inflammatory exposure. IL?6, IL?6 receptor
(IL?6R) and glycoprotein 130 expression was detected by immunohistochemistry. In
addition, an ELISA was performed to quantify the levels of soluble IL?6R (sIL?6R)
in the cystic fluid and supernatants of ACP cells and tumor?associated
fibroblasts. These measurements demonstrated that ACP cells produce IL?6 and its
associated proteins. In addition, the results revealed that while the viability
of ACP cells was not affected, the migration of ACP cells was promoted by IL?6
treatment in a concentration?dependent manner. Conversely, treatment with an
IL?6?blocking monoclonal antibody significantly decreased the migration of ACP
cells. In addition, IL?6 treatment increased the expression of vimentin and
decreased the expression of E?cadherin in a dose?dependent manner. The findings
of the present study demonstrate that IL?6 may promote migration in vitro via the
classic? and trans?signaling pathways by inducing epithelial?mesenchymal
transition in ACP cell cultures.