Objective      To investigate the effect and mechanism of microRNA-32 (miR-32) regulation on the proliferation and apoptosis of esophageal carcinoma(EC) cell line KYSE-410. Methods      Quantitative real-time PCR (qRT-PCR) was used to detect the expression level of miR-32 in EC tissues of 47 patients and 7 EC cell lines. Dual-luciferase reporter assay was used to exam the binding site of 3′ UTR-PTEN to miR-32

which PTEN was theoretically predicted as downstream target of miR-32 by TargetScan database. KYSE-410 cells were either transfected with miR-32 mimics alone or co-transfected with miR-32 and constructed PTEN plasmid for PTEN rescue experiment. The regulation role of miR-32 on PTEN mRNA and protein expression

proliferation and apoptosis were assessed by Western blotting

MTT assay and Annexin V-FITC apoptosis detection kit

respectively. PTEN rescue experiment was used to validate the effect of miR-32 on PTEN expression.  Results       The expression of miR-32 was significantly increased in 89% (42/47 patients) EC tissues compared with corresponding adjacent normal tissues

and was highest in low differentiated KYSE-410 cells (P0.05). Dual-luciferase reporter assay showed that upregulation of miR-32 decreased luciferase activity of 3′ UTR-PTEN

suggesting that PTEN was the functional downstream target of miR-32. In KYSE-410 cells

overexpression of miR-32 promoted the proliferation

inhibited the apoptosis (inhibitory rate 28%

P0.05)

and suppressed PTEN protein expression (inhibitory rate 48%

P0.05)

but had no change in mRNA level. Compared to cells transfected with miR-32 mimics alone

co-transfected cells (PTEN+miR-32 mimics) could partly reverse the inhibitory effect of miR-32 on PTEN protein expression and apoptosis. The proliferation rate was significantly decreased at 96 h

and no differences were seen at other measured time points between PTEN+miR-32 and miR-32 transfected KYSE-410 cells. Conclusions       MiR-32 can promote the proliferation of esophageal carcinoma at least in part by suppression of PTEN expression.