Objective : To investigate the expression and prognosis of protein regulator of cytokinesis 1 ( PRC1) in pancreatic carcinoma tissues．Moreover，to explore the effects of PRC1 on the biological functions of pancreatic carcinoma cell line SW1990 and its related mechanisms． Methods: The GEPIA database was used to analyze the expression difference of PRC1 in pancreatic carcinoma tissues and normal pancreatic tissues．Overexpression and interference of PRC1 were achieved by Lipofectamine 3000 transfection plasmid or shRNA method．Then CCK-8 assay，Transwell assay and flow cytometry were used to detect the proliferation level，invasion ability and apoptosis of the SW1990 cells，respectively．The pancreatic carcinoma data were collected from the Cancer Genome Atlas (TCGA) database．The correlation between expression level of PRC1 and clinicopathological features of pancreatic carcinoma was analyzed．The STRING database was used to analyze the network of proteins interacting with PRC1 . Gene set enrichment analysis ( GSEA) was used to predict the possible signal pathways of PRC1 in pancreatic car- cinoma. Results: GEPIA database results showed that PRC1 expression in pancreatic carcinoma tissue was higher than that in normal pancreatic tissue (P＜0．05) ．The results of CCK-8 assay，Transwell assay and flow cytometry showed that PRC1 overexpression significantly enhanced SW1990 cell proliferation，invasion and inhibited apoptosis (P＜0. 01) ．Whereas PRC1 interference significantly inhibited SW1990 cell proliferation，invasion and enhanced apoptosis (P＜0. 01) ．TCGA database data analysis identified PRC1 mRNA expression level and M stage were independent risk factors affecting the prognosis of pancreatic carcinoma (P＜0. 05) ．STRING database showed that there was an interaction between PRC1 and PLK1 and so on．GSEA research results showed that the PRC1 mRNA high expression samples were enriched into P53 signaling pathway and so on (P＜0. 05) ． Conclusion PRC1 is highly expressed in pancreatic carcinoma，and it is associated with proliferation，invasion，apoptosis and prognosis of pancreatic carcinoma．Moreover，it plays an important role in pancreatic carcinoma by regulating interacting proteins PLK1 and activating P53 signaling pathways.

Objective : To investigate the effects of actin like 6A (ACTL6A) knockdown on the proliferation, apop⁃ tosis, migration and invasion of SW1990 cells in pancreatic cancer. Methods : The Oncomine database was used to analyze the expression of ACTL6A mRNA in the tissues of pancreatic cancer and normal pancreas. The plasmid of knockdown ACTL6A and siRNA negative control were established and transfected into SW1990 cell line as siRNA⁃ACTL6A group and siRNA⁃NC group. CCK⁃8, cell apoptosis experiment, Wound healing and Transwell assay were used to determine the effects of ACTL6A knockdown on the proliferation, apoptosis, migration and invasion of SW1990 cells. GSEA predicted a possible pathway regulated by ACTL6A in pancreatic cancer. T⁃test was used between the two groups. Results : The expression of ACTL6A in pancreatic cancer tissues was higher than that in normal pancreatic tissues ( P < 0. 05 ) . The results of CCK⁃8 assay showed that the absorbance of siRNA⁃ACTL6A group at 24 and 48 h were lower than those in the siRNA⁃NC group, and the difference was statistically significant ( t = 5. 840, 8. 454, P < 0. 01) . The results of Wound healing assay and Transwell assay showed that the healing rate and the number of invasive cells in siRNA⁃ACTL6A group were both lower than those in the siRNA⁃NC group. The difference was statistically significant ( t = 3. 960,4. 464, P < 0. 05), but the apoptosis rate of siRNA⁃ACTL6A group was significantly higher than that of the siRNA⁃NC group, and the difference was statistically significant( t = 12. 192, P < 0. 001) . GSEA results showed that the group with high expression of ACTL6A mRNA was up⁃regulated in cell cycle, nucleotide excision repair, base excision repair, DNA replication, pathways in cancer, NOTCH signaling pathway and other related gene sets(P < 0. 05) . These pathways were activated when the expression of ACTL6A was up⁃regulated. Conclusion ACTL6A is highly expressed in pancreatic cancer tissues. ACTL6A knockdown promotes the cell apoptosis of SW1990 cells, and inhibits proliferation, invasion and migration of SW1990 cells. The mechanism of the occurrence and development of ACTL6A in pancreatic cancer is attributed to the activation of cell cycle, nucleotide excision repair, base excision repair, DNA replication, pathways in cancer, NOTCH signaling pathway.