MicroRNA-543 controls pancreatic cancer development by LINC00847-microRNA-543-STK31 axis

Abstract Background Pancreatic cancer (PC) is one of the most malignant cancers of the gastro-intestinal tract. However, the study of targeted immunity in pancreatic cancer is not very thorough. Therefore, targeted molecular markers are needed to solve the diagnosis and treatment of pancreatic cancer. Methods In our research, we investigated the biological functions and molecular mechanism of microRNA-543 in PC. qRT-PCR and western blotting (WB) was utilized to test the transcription of microRNA-543, STK31, and LINC00847 in BxPC-3 as well as PANC-1cells. Then CCK-8, Trans-well, colony formation assay and flow cytometry assay were utilized to detect cell growth in cell number, migration, invasion and apoptosis, WB and FISH were utilized to evaluate the epithelial–mesenchymal transition (EMT) process and cellular subcellular localization. RIP, double luciferase report and RNA-pull down assay were utilized to determine targeting relationship between microRNA-543 and STK31 or microRNA-543-LINC00847. Results While microRNA-543 transcription was discovered to be low in PC, LINC00847 and STK31 were overexpressed at significant levels. MicroRNA-543 knockdown dramatically increased PC cell growth in cell number, invasion, metastasis, and EMT, as well as decreased apoptosis, in functional research. Furthermore, microRNA-543 and STK31 are mutually targeted. LINC00847 worked as a molecular absorbent for microRNA-543, and a competitive endogenous RNA (ceRNA) for STK31, increasing STK-31 transcription. Conclusions We believe that microRNA-543, through the LINC00847-microRNA-543-STK31 axis, plays a role in the development of PC and that it is a tumor suppressor as well. As a result, MicroRNA-543 may prove to be an impactive diagnostic and therapeutic target in this illness.