Issue 66, 2018

Retracted Article: Long non-coding RNA KCNQ1OT1 promotes osteosarcoma progression by increasing β-catenin activity

Abstract

Objective: Long non-coding RNA KCNQ1OT1 has been associated with the development of different types of cancers. The present research investigated the role of KCNQ1OT1 in osteosarcoma. Methods: Expression level of KCNQ1OT1 in osteosarcoma and paired non-cancerous tissue specimens from 56 osteosarcoma patients and its association with patients' clinicopathological features was investigated. KCNQ1OT1 overexpression and knockdown in primary-cultured osteosarcoma cells was constructed by lentiviral transduction. Influence of KCNQ1OT1 overexpression or knockdown on osteosarcoma cell growth, apoptosis, migration, invasion, epithelial-to-mesenchymal transition and beta-catenin activation was investigated. Results: Expression of KCNQ1OT1 in osteosarcoma tissue specimens was significantly increased in comparison to that in adjacent counterparts. High expression of KCNQ1OT1 significantly associated with osteosarcoma progression and patients' decreased survival. Overexpression of KCNQ1OT1 significantly increased osteosarcoma cell growth, proliferation, migration, invasion, epithelial-to-mesenchymal transition and beta-catenin activation while reducing cell apoptosis in vitro, and KCNQ1OT1 knockdown showed opposite effects. Inhibition of beta-catenin/TCF activity by ICG-001 treatment significantly attenuated the promoting effect of KCNQ1OT1 overexpression on osteosarcoma cell malignancy described above. Conclusion: KCNQ1OT1 might be a potential prognostic factor in osteosarcoma. High expression of KCNQ1OT1 might promote osteosarcoma development by increasing the activation of WNT/beta-catenin signaling pathway.

Graphical abstract: Retracted Article: Long non-coding RNA KCNQ1OT1 promotes osteosarcoma progression by increasing β-catenin activity

Associated articles

Article information

Article type
Paper
Submitted
29 Aug 2018
Accepted
07 Oct 2018
First published
08 Nov 2018
This article is Open Access
Creative Commons BY-NC license

RSC Adv., 2018,8, 37581-37589

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