OBJECTIVES: There have been no previous reports concerning functions of miR-103a in gastric cancer (GC) cells. Thus the aim of the study was to investigate its expression and role in development of this tumour. MATERIALS AND METHODS: Real-time RT-PCR was performed to detect expression of miR-103a in GC cell lines and clinical cancer specimens. To further understand its role, we restored expression of miR-103a in MGC-803 cell line by transfection with miR-103a mimics or inhibitors. Effects of miR-103a on cell proliferation, migration and invasion on targets were also determined. RESULTS: miR-103a was down-regulated in both GC cell lines and clinical cancer specimens. Meanwhile, its level was closely associated with pM or pTNM stage of GC. Overexpression of miR-103a markedly suppressed proliferation, migration, and invasion of GC cells, while its inhibition significantly accelerated cell proliferation, migration and invasion. Moreover, c-Myb was identified to be a functional downstream target of miR-103a, ectopic expression of which partially reversed suppression of cell proliferation and invasion. CONCLUSIONS: Thus our observations suggest that miR-103a functioned as a tumour suppressor by targeting c-Myb. These findings indicate that miR-103a might play a significant role in pathogenesis of GC.
OBJECTIVES: There have been no previous reports concerning functions of miR-103a in gastric cancer (GC) cells. Thus the aim of the study was to investigate its expression and role in development of this tumour. MATERIALS AND METHODS: Real-time RT-PCR was performed to detect expression of miR-103a in GC cell lines and clinical cancer specimens. To further understand its role, we restored expression of miR-103a in MGC-803 cell line by transfection with miR-103a mimics or inhibitors. Effects of miR-103a on cell proliferation, migration and invasion on targets were also determined. RESULTS:miR-103a was down-regulated in both GC cell lines and clinical cancer specimens. Meanwhile, its level was closely associated with pM or pTNM stage of GC. Overexpression of miR-103a markedly suppressed proliferation, migration, and invasion of GC cells, while its inhibition significantly accelerated cell proliferation, migration and invasion. Moreover, c-Myb was identified to be a functional downstream target of miR-103a, ectopic expression of which partially reversed suppression of cell proliferation and invasion. CONCLUSIONS: Thus our observations suggest that miR-103a functioned as a tumour suppressor by targeting c-Myb. These findings indicate that miR-103a might play a significant role in pathogenesis of GC.
Authors: Michal Tichý; Lucia Knopfová; Jiří Jarkovský; Lucie Pekarčíková; Lenka Veverková; Petr Vlček; Jana Katolická; Ivan Čapov; Markéta Hermanová; Jan Šmarda; Petr Beneš Journal: Tumour Biol Date: 2016-02-12