Long non-coding RNA XIST promotes the development of esophageal cancer by sponging miR-494 to regulate CDK6 expression - 09/12/18
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Graphical abstract |
Highlights |
• | Highly expression of XIST was obtained in esophageal cancer tissues and cells. |
• | XIST promoted the malignant behaviors of esophageal cancer cells. |
• | XIST may sponge miR-494 to play a significant role in esophageal cancer. |
• | CDK6 was a target of miR-494 to mediate the role of miR-494 in esophageal cancer. |
• | CDK6 knockdown could inhibit the activation of JAK2/STAT3 pathway. |
Abstract |
Objective |
Esophageal cancer is one of the deadliest cancers worldwide occurring at upper gastrointestinal tract. This study aimed to explore the possible role of long non-coding RNA X Inactive Specific Transcript (XIST) in the development of esophageal cancer.
Material and methods |
The lncRNA XIST expressions both in esophageal cancer tissues and in cells were investigated. The TE-1 and SKGT-4 cells were transfected with LV-sh-XIST and LV-scramble for the further detection of the effects of XIST expression on cell biological processes, including proliferation, apoptosis and the expression of apoptosis-related proteins, migration, invasion and the expression of epithelial-mesenchymal transition markers. Additionally, the regulatory relationships between lncRNA XIST and miR-494, between miR-494 and CDK6, between miR-494/CDK6 and JAK2/STAT3 pathway were investigated.
Results |
LncRNA XIST was overespressed in esophageal cancer tissues and cells. Suppression of XIST significantly inhibited the proliferation, migration and invasion, but induced apoptosis of two kinds of cells, TE-1 and SKGT-4. Moreover, miR-494 was down-regulated in esophageal cancer tissues and cells. XIST could sponge miR-494 and inhibition of miR-494 reversed the effects of XIST suppression on the malignant behaviors of TE-1 cells. Also, CDK6 was a target of miR-494 and CDK6 knockdown reversed the effects of miR-494 inhibition on the malignant behaviors of TE-1 cells. Besides, the expression of p-JAK2 and p-STAT3 was increased after miR-494 inhibition, which was reversed after inhibition of miR-494 and CDK6 at the same time.
Conclusions |
The data presented in this study revealed that XIST abnormal expression may play an oncogenic role in the development of esophageal cancer via miR-494/CDK6 axis through JAK2/STAT3 signal pathway. This study may provide theoretical basis for the molecular mechanism investigation of esophageal cancer.
Le texte complet de cet article est disponible en PDF.Keywords : Esophageal cancer, Long non-coding RNA, X inactive specific transcript, miR-494, Cyclin dependent kinase 6 (CDK6), JAK2/STAT3 pathway
Plan
Vol 109
P. 2228-2236 - janvier 2019 Retour au numéro
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