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10.1002/2211-5463.12215

http://scihub22266oqcxt.onion/10.1002/2211-5463.12215
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suck abstract from ncbi


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pmid28680805
      FEBS+Open+Bio 2017 ; 7 (7 ): 905-914
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  • miR-944 inhibits metastasis of gastric cancer by preventing the epithelial-mesenchymal transition via MACC1/Met/AKT signaling #MMPMID28680805
  • Pan T ; Chen W ; Yuan X ; Shen J ; Qin C ; Wang L
  • FEBS Open Bio 2017[Jul]; 7 (7 ): 905-914 PMID28680805 show ga
  • MicroRNAs (miRNAs) are reported to play vital roles in tumor progression. Recently, miR-944 was reported to play either an oncogenic or tumor suppressive role in human cancers. However, the expression of miR-944 and its exact role in gastric cancer (GC) remain unknown. This study aimed to evaluate whether loss of miR-944 could promote the epithelial-mesenchymal transition (EMT) of GC. Reduced expression of miR-944 was identified in 40 pairs of human GC and matched normal tissues by qRT-PCR. Reduced expression of mi-944 was also observed in GC cell lines. Restoration of miR-944 inhibited cell migration and invasion in MGC-803 cells, while its loss facilitated metastasis of SGC-7901 and BGC-823 cells. Notably, miR-944 overexpression prohibited EMT of GC cells in vitro, while miR-944 knockdown had the opposite effect. Bioinformatics software predicted that MACC1 was a direct target of miR-944. We observed negative regulation of miR-944 on MACC1 expression, and direct binding between miR-944 and MACC1 was verified by dual-luciferase assays in HEK293T cells. Restoration of MACC1 resulted in promoted EMT and metastasis in miR-944-overexpressing MGC-803 cells. Loss of MACC1 abrogated the effects of miR-944 knockdown on EMT and metastasis of SGC-7901 cells. We also found that the Met-AKT pathway might be involved in MACC1-mediated EMT. In conclusion, miR-944 acts as an inhibitor of EMT and metastasis of GC by targeting MACC1. This study highlights the potential effects of miR-944 in the prognosis and treatment of GC.
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