MiRNA-339-5p suppresses the malignant development of gastric cancer via targeting ALKBH1

To uncover the role of microRNA-339-5p (miRNA-339-5p) in the development of gastric cancer (GC) and its possible molecular mechanism. Differential expressions of miRNA-339-5p in GC and adjacent normal tissues were detected. The relationship between miRNA-339-5p level and clinical features in GC pati...

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Published inExperimental and molecular pathology Vol. 115; p. 104449
Main Authors Wang, Chenchen, Huang, Yakai, Zhang, Jieyun, Fang, Yantian
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.08.2020
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ISSN0014-4800
1096-0945
1096-0945
DOI10.1016/j.yexmp.2020.104449

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Summary:To uncover the role of microRNA-339-5p (miRNA-339-5p) in the development of gastric cancer (GC) and its possible molecular mechanism. Differential expressions of miRNA-339-5p in GC and adjacent normal tissues were detected. The relationship between miRNA-339-5p level and clinical features in GC patients was analyzed. Proliferative and migratory changes in BGC-823 and SGC-7901 cells overexpressing miRNA-339-5p were examined. Finally, luciferase assay and rescue experiments were conducted to explore the regulatory mechanism of miRNA-339-5p in its downstream gene ALKBH1, and their interaction in the development of GC. MiRNA-339-5p was downregulated in GC tissues. Lowly expressed miRNA-339-5p was unfavorable to prognosis in GC because of high rates of lymphatic metastasis and distant metastasis. Overexpression of miRNA-339-5p markedly reduced proliferative and migratory abilities in GC cells. ALKBH1 was identified to be the downstream gene of miRNA-339-5p. In GC tissues, ALKBH1 was upregulated and negatively correlated to miRNA-339-5p level. Overexpression of ALKBH1 was able to reverse the inhibitory effects of overexpressed miRNA-339-5p on proliferative and migratory abilities in GC. Lowly expressed miRNA-339-5p is closely related to metastasis and poor prognosis in GC patients. MiRNA-339-5p suppresses the malignant development of GC by negatively regulating ALKBH1.
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ISSN:0014-4800
1096-0945
1096-0945
DOI:10.1016/j.yexmp.2020.104449