Open Access
ARTICLE
LINC00052 Promotes Gastric Cancer Cell Proliferation and Metastasis via Activating the Wnt/β-Catenin Signaling Pathway
Department of General Surgery, Hangzhou First People’s Hospital, Hangzhou, P.R. China
1 These authors provided equal contribution to this work
Oncology Research 2017, 25(9), 1589-1599. https://doi.org/10.3727/096504017X14897896412027
Retracted 05 September 2024
A retraction of this article was approved in:
Retraction: LINC00052 promotes gastric cancer cell proliferation and metastasis via activating the Wnt/β-Catenin signaling pathway
Read retraction
Abstract
Gastric cancer (GC) is one of the most common malignant tumors of the digestive system. The etiology of GC is complex, and much more attention should be paid to genetic factors. In this study, we explored the role and function of LINC00052 in GC. We applied qRT-PCR and Northern blot to detect the expression of LINC00052 and found it was highly expressed during GC. We also investigated the effects of LINC00052 on tumor prognosis and progression and found that LINC00052 indicated poor prognosis and tumor progression. By performing MTT, colony formation, and Transwell assays, we found that LINC00052 promoted MGC- 803 cell proliferation and metastasis. Pull-down and RIP assays showed that LINC00052 could interact with β-catenin and methyltransferase SMYD2, and immunoprecipitation detection showed that LINC00052 promoted β-catenin methylation to maintain its stability, so as to activate the Wnt/β-catenin pathway. Furthermore, XAV939 (inhibitor of β-catenin) was used to treat MGC-803 cells, and we found that LINC00052 promoted proliferation and metastasis, possibly by activation of the Wnt/β-catenin pathway. In conclusion, our research demonstrated a carcinogenic role for LINC000052 in GC, which may represent a new approach for the prevention and therapy of this cancer.Keywords
Cite This Article
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.