IL-1β induced RXRα overexpression through activation of NF-κB signaling in gastric carcinoma

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• 作者：Hong-Yue Ren^a ; ¹ ; Gui-Li Huang^b ; ¹ ; Wen-Ming Liu^c ; ¹ ; Wei Zhang^d ; Yu Liu^a ; Guo-Qiang Su^a ; ; Dong-Yan Shen^a ; ^{shendongyan@163.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：RXRα ; Gastric carcinoma ; IL-1β ; NF-κB
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：78
• 期：Complete
• 页码：329-334
• 全文大小：1657 K

文摘

Abnormal expression of Retinoid X Receptor α (RXRα) seems to be a frequent incident in a variety of cancers. However, the expression pattern and the mechanisms in gastric carcinoma (GC) remain unclear.

Methods

In GC tissues and cell lines, the expression levels of RXRα mRNA and protein were detected by Q-PCR and Western blot, respectively; the localization of RXRα was evaluated by immunohistochemistry (IHC) or immunocytochemistry (ICC). The effect of IL-1β on RXRα expression and localization was detected by Western blot and ICC. Nuclear factor-κB (NF-κB) pathway was assessed via Western blot.

Results

RXRα expression was markedly elevated at both mRNA and protein levels in GC tissues and cell lines (all P < 0.05). The abnormal overexpression of RXRα was predominantly visualized in cytoplasm. IL-1β significantly induced cytoplasmic expression of RXRα in a time-dependent manner. Co-incubation with IL-1β enhanced phospho-IKKα (p-IKKα) expression and this effect could be inhibited by the specific inhibitor for NF-κB (all P < 0.01).

Conclusions

IL-1β upregulated RXRα through activation of NF-κB signaling and these suggested a possible clinic significance of retinoid receptor expression in the diagnosis and treatment of GC.