Background and purpose: Gastric cancer is one of the common malignant tumors in the digestive system

but its pathogenesis is not clear. Diaphanous-related formin 3 (DIAPH3) plays an important role in the occurrence and development of a variety of tumors

however

its role in gastric cancer has not been reported. This study was to investigate the expression of DIAPH3 in gastric cancer and its effect on the proliferation

migration and invasion of gastric cancer cells. Methods: Gene expression profiling interactive analysis (GEPIA) database was used to analyze the expression of DIAPH3 in gastric cancer. Paraffin embedded tissues and paired adjacent tissues from 62 patients with gastric cancer were collected. The expression of DIAPH3 in gastric cancer was detected by immunohistochemistry

and the clinicopathological correlation was analyzed. Western blot was performed to detect the effects of knockdown or over-expression of DIAPH3 on the protein levels of DIAPH3

cyclin D1

E-cadherin

vimentin and N-cadherin. Real- time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the effect of knockdown or over-expression of DIAPH3 mRNA. Cell proliferation was detected by cell counting kit-8 (CCK-8). Cell migration was detected by the wound healing assay

and cell invasion was detected by transwell chamber experiment. Results: GEPIA database online predicted that the expression of DIAPH3 mRNA was higher in gastric cancer than in adjacent non-cancer tissues (P＜0.05). The positive expression rate of DIAPH3 in gastric cancer was 70.97% (44/62)

which was higher than that in adjacent non-cancer tissues (16.13%

10/62

 P＜0.01). Compared with the high differentiation group

the expression of DIAPH3 in the low differentiation group was higher (P＜0.05). Compared with the group without lymph node metastasis

the expression of DIAPH3 in the group with lymph node metastasis was higher (P＜0.05). The cell proliferation activity

cell migration rate and cell invasion were lower in the interference DIAPH3 group than in the negative control group (P＜0.05). The cell proliferation activity

cell migration rate and cell invasion number were higher in the over-expression of DIAPH3 group than in the over-expression control group (P＜0.05). Following over- expression of DIAPH3 and interference of cyclin D1

the proliferation activity of gastric cancer cell line was lower compared with over-expression of DIAPH3 group and higher compared with over-expression control group (P＜0.05). Following over-expression of DIAPH3 and interference of vimentin

the cell migration rate and cell invasion number of gastric cancer cell line were lower compared with over-expression DIAPH3 group and higher compared with over-expression control group (P＜0.05). Compared with the interference control group

the expression of E-cadherin protein increased

and the expressions of DIAPH3

cyclin D1

vimentin and N-cadherin decreased in the interference DIAPH3 group (P＜0.05). Compared with the control group

the expression of E-cadherin protein decreased

and the protein expressions of DIAPH3

cyclin D1

vimentin and N-cadherin increased in the over-expression group. In knockdown or over-expression of DIAPH3 gastric cancer cell lines

the mRNA level of DIAPH3 decreased or increased significantly (P＜0.05). Conclusion: DIAPH3 promotes the proliferation

migration and invasion of gastric cancer cells. The role of DIAPH3 is associated with up-regulation of cyclin D1 and epithelial-mesenchymal transition.