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. 2017 Oct 31;41(1):155–163. doi: 10.3892/ijmm.2017.3225

Figure 3.

Figure 3

Histone deacetylase 3 (HDAC3) regulates miR-454 expression and the role of miR-454 in gastric cancer (GC) tumorgeneisis. (A) HDAC3 overexpression upregulated miR-454 expression by microarray analysis. HDAC1-1, HDAC1-2 and HDAC1-3; Vector-1, Vector-2 and Vector-3 refer to the cDNA microarray results of triplicate experiments. Green and red color intensity refers to downregulation and upregulation, respectively. (B) Linear regression analysis revealed that the miR-454 level significantly and positively correlated with HDAC3 expression. miR-454 mRNA expression was significantly upregulated (C) in GC cell lines and (D) tissues compared with normal cell/non-tumor tissues. (E) Patients with a high expression of miR-454 had a markedly worse survival percentage compared to those with a low miR-454 level. (F) In 33 cases presenting advanced disease (stages of III and IV), 21 (63.64%) of the cases had a high level miR-454 expression in GC tissue; whereas in 27 cases with early stage disease (stages I and II), only 8 (29.63%) presented high levels of miR-454 expression. (G) In the 33 cases of GC with lymph node metastasis, 24 (72.73%) presented a high miR-454 expression, while only 5 (18.52%) of 27 cases of BC without lymph node metastasis present high level miR-454 expression. (H) miR-454 knockdown significantly inhibited the viability of (H) AGS and (I) SGC-7901 cells. Cell viability was detected in GC cell lines following culture for 0, 24, 48 and 72 h. Optical density was measured at a wavelength of 450 nm. Data are presented as the means ± SEM. *p<0.05, **p<0.01 and ***p<0.001 vs. normal cells or si-cont.