Open AccessLINC00052 Promotes Gastric Cancer Cell Proliferation and Metastasis via Activating the Wnt/β-Catenin Signaling Pathway
Author(s) -
Yuqiang Shan,
Rongchao Ying,
Jia Zhong,
Wencheng Kong,
Yi Wu,
Shuier Zheng,
Huicheng Jin
Publication year - 2017
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504017x14897896412027
Subject(s) - wnt signaling pathway , cancer research , metastasis , catenin , cell growth , cancer , biology , carcinogenesis , immunoprecipitation , western blot , mtt assay , signal transduction , cell culture , microbiology and biotechnology , genetics , gene
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.