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Association of HOTAIR expression with PI3K/Akt pathway activation in adenocarcinoma of esophagogastric junction

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Abstract Objectives Although the Hox transcript antisense intergenic RNA (HOTAIR), a vital long non-coding RNA, is known to participate in the development and progression of a wide range of carcinomas, there are still no published reports regarding its expression in adenocarcinoma of esophagogastric junction (AEJ). The aims of this study were to investigate the expression of HOTAIR, and to analyze the association of its expression with PI3K/Akt pathway activation in clinical AEJ patients. Methods Nine normal epithelial tissues and 41 samples of AEJ were studied comparably. The expression of HOTAIR was detected by real-time PCR according to the different tumor grades in these AEJ tissues. Western blot was performed to reveal the Ser473-phosphorylated Akt and total Akt levels. Results: HOTAIR was found to be up-regulated in higher grades of AEJ tissues compared to low grades and/or noncancerous tissues. pAkt expression was also found to be up-regulated in tissues of higher tumor stages. We found that the overexpression of HOTAIR finely correlated with elevated Ser473-phosphorylated Akt levels. Conclusion: Upregulated HOTAIR was associated with abnormal activated PI3K/Akt pathway, which might serve as a promising therapeutic strategy for AEJ treatment.
Title: Association of HOTAIR expression with PI3K/Akt pathway activation in adenocarcinoma of esophagogastric junction
Description:
Abstract Objectives Although the Hox transcript antisense intergenic RNA (HOTAIR), a vital long non-coding RNA, is known to participate in the development and progression of a wide range of carcinomas, there are still no published reports regarding its expression in adenocarcinoma of esophagogastric junction (AEJ).
The aims of this study were to investigate the expression of HOTAIR, and to analyze the association of its expression with PI3K/Akt pathway activation in clinical AEJ patients.
Methods Nine normal epithelial tissues and 41 samples of AEJ were studied comparably.
The expression of HOTAIR was detected by real-time PCR according to the different tumor grades in these AEJ tissues.
Western blot was performed to reveal the Ser473-phosphorylated Akt and total Akt levels.
Results: HOTAIR was found to be up-regulated in higher grades of AEJ tissues compared to low grades and/or noncancerous tissues.
pAkt expression was also found to be up-regulated in tissues of higher tumor stages.
We found that the overexpression of HOTAIR finely correlated with elevated Ser473-phosphorylated Akt levels.
Conclusion: Upregulated HOTAIR was associated with abnormal activated PI3K/Akt pathway, which might serve as a promising therapeutic strategy for AEJ treatment.

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