mi R-1181 inhibits invasion and proliferation via STAT3 in pancreatic cancer

AIM To examine the role of microRNA 1181 (miR-1181) in invasion and proliferation in pancreatic cancer. METHODS We analyzed the expression of miR-1181 in several pancreatic cancer cell lines and generated stable MIA- PaCa- 2 and PANC-1 cell lines with up-regulated miR-1181 expression using an adenovirus delivery system. We then investigated miR-1181 ' s effect on invasion and proliferation of pancreatic cancer cells by transwell assay, wound healing assay, cell counting kit-8 assay and colony-forming assay, and explored any underlying mechanisms by western bolt. Beyond that, we observed the change of the PANC-1 cell ' s cytoskeleton by immunofluorescence staining. RESULTS Our data showed that miR-1181 was relatively downregulated in pancreatic cancer cell lines compared with normal pancreatic ductal epithelial cells. And miR-1181 inhibited the migration, invasion and proliferation activities of MIA-PaCa-2 and PANC-1 cells. Notably,after over-expressing of miR-1181 in PANC-1 cells, F-actin depolymerized. Immunofluorescence staining shows decreased F-actin and beta-tubulin expression in PANC-1 cells over-expressing miR- 1181 compared with the control cells. Furthermore, we found that over-expressing miR- 1181 inhibited the expression of signal transducer and activator of transcription 3(STAT3) while knocking- down miR-1181 up-regulated the expression of STAT3. Knocking-down miR-1181 promoted the invasion and proliferation of pancreatic cancer cells. And inhibition of STAT3 blocked the promotion effects of knocking- down miR-1181 on proliferation and invasion in pancreatic cancer. CONCLUSION Together our findings suggest that miR-1181 may be involved in pancreatic cancer cell invasion and proliferation by targeting STAT3 and indicate that miR-1181 may be a potential therapeutic agent for pancreatic cancer.

AIM To examine the role of micro RNA 1181(miR-1181) ininvasionandproliferationinpancreaticcancer.METHODS We analyzed the expression of mi R-1181 in severalpancreatic cancer cell lines and generated stableMIA-Pa Ca-2 and PANC-1 cell lines with up-regulatedmi R-1181 expression using an adenovirus deliverysystem. We then investigated mi R-1181's effect oninvasion and proliferation of pancreatic cancer cells bytranswell assay, wound healing assay, cell countingkit-8 assay and colony-forming assay, and exploredany underlying mechanisms by western bolt. Beyondthat, we observed the change of the PANC-1 cell'scytoskeletonbyimmunofluorescencestaining.RESULTS Our data showed that mi R-1181 was relatively downregulatedinpancreaticcancercelllinescomparedwithnormalpancreaticductalepithelialcells.AndmiR-1181inhibited the migration, invasion and proliferationactivities of MIA-Pa Ca-2 and PANC-1 cells. Notably,after over-expressing of mi R-1181 in PANC-1 cells,F-actin depolymerized. Immunofluorescence stainingshows decreased F-actin and β-tubulin expression inPANC-1 cells over-expressing mi R-1181 comparedwith the control cells. Furthermore, we found thatover-expressing mi R-1181 inhibited the expressionof signal transducer and activator of transcription 3(STAT3) while knocking-down mi R-1181 up-regulatedthe expression of STAT3. Knocking-down mi R-1181promoted the invasion and proliferation of pancreaticcancer cells. And inhibition of STAT3 blocked thepromotion effects of knocking-down mi R-1181 onproliferationandinvasioninpancreaticcancer.CONCLUSION Together our findings suggest that mi R-1181 maybe involved in pancreatic cancer cell invasion andproliferation by targeting STAT3 and indicate thatmi R-1181 may be a potential therapeutic agent forpancreaticcancer.