4.7 Article

Tumor suppressor miR-24 restrains gastric cancer progression by downregulating RegIV

期刊

MOLECULAR CANCER
卷 13, 期 -, 页码 -

出版社

BMC
DOI: 10.1186/1476-4598-13-127

关键词

miR-24; RegIV; Gastric cancer; Proliferation; Invasion; Metastasis

资金

  1. National Natural Science Foundation of China [81272749, 81172324, 91229106]
  2. Science and Technology Commission of Shanghai Municipality [11441902100, 12XD1403700, 13ZR1425600]
  3. Key Projects in the National Science & Technology Pillar Program of China [2014BAI09B03]
  4. Research Fund for the Doctoral Program of Higher Education of China [20110073110071]

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Background: microRNAs are small noncoding RNAs that modulate a variety of cellular processes by regulating multiple targets, which can promote or inhibit the development of malignant behaviors. Accumulating evidence suggests miR-24 plays important roles in human carcinogenesis. However, its precise biological role remains largely elusive. This study examined the role of miR-24 in gastric cancer (GC). Methods: The expression of miR-24 in GC tissues compared with matched non-tumor tissues and GC cells was detected by qRT-PCR. Synthetic short single or double stranded RNA oligonucleotides and lentiviral vectors were used to regulate miR-24 expression in GC cells to investigate its function in vitro and in vivo. Results: miR-24 was significantly downregulated in GC tissues compared with matched non-tumor tissues and was associated with tumor differentiation. Ectopic expression of miR-24 in SGC-7901 GC cells suppressed cell proliferation, migration and invasion in vitro as well as tumorigenicity in vivo by inducing cell cycle arrest in G0/G1 phase and promoting cell apoptosis. Furthermore, we identified RegIV as a target of miR-24 and demonstrated that miR-24 regulated RegIV expression via binding its 3' untranslated region. Conclusions: miR-24 functions as a novel tumor suppressor in GC and the anti-oncogenic activity may involve its inhibition of the target gene RegIV. These findings suggest the possibility for miR-24 as a therapeutic target in GC.

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