Effect of tRF-Pro-CGG on the biological behavior of mouse pancreatic cancer cells and its molecular mechanism

Background and purpose: tRNA-derived fragments (tRF) are a kind of short non-coding RNA (14-30 nt) that influences the course of cancer. This study aimed to investigate the molecular pathways that might underlie the effects of tRF-Pro-CGG on the biological behavior of mouse pancreatic cancer cells. Methods: Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to assess the expression of tRF-Pro-CGG in mouse pancreatic cancer cell lines pan02 and LTPA, human pancreatic cancer cell line Capan-2, and normal pancreatic cells HPDE6-C7. tRF-Pro-CGG overexpression in pan02 cells and LTPA cell suppression were achieved through lentiviral transfection, and RTFQ-PCR and Western blot were used to determine overexpression and knockdown effects. Cell counting kit-8 (CCK-8) was used to detect cell proliferation. Transwell assays were used to detect cell migration and invasion ability. The effect of tRF-Pro-CGG on the growth and metastasis of pancreatic cancer transplantation tumors in nude mice model was investigated. H-E staining was used to observe the histopathological structure of transplantation tumors. Western blot was used to detect the expression and phosphorylation of proliferation-related protein Ki-67 and metastasis-related proteins. Western blot was used to assess the expressions of cadherin, vimentin, phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway protein and phosphorylation in transplanted tumor tissues. Results: tRF-Pro-CGG expression was lowest in the mouse pancreatic cancer cell line pan02. Both mRNA and protein expression levels of tRF-Pro-CGG were significantly increased (P