Thioredoxin-interacting protein is a favoredtarget of miR-125b, promoting metastasis and progression of pancreatic cancer via the HIF1α pathway.

Abstract

MicroRNAs (miRs) are vital in the development of pancreatic cancer (PC) targeting several cellular processes. Thisstudy was aimed atevaluating the function of miR-125b and the mechanism involved in PC.Cell migration, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), and Bromodeoxyuridine/5-bromo-2'-deoxyuridine (BrdU) study was done to establish the migration capability, cell viability, and cell proliferation, respectively. Binding sites for miR-125b were recognized by luciferase assay, and the expression of protein by Western blot and immunofluorescence assay. In vivo study was done by BALB/c nude xenograft mice for evaluating the function of miR-125b.The study showed that expression of miR-125b was elevated in PC cells and tissuesand was correlated to proliferation and migration of cells. Also, overexpression of miR-125b encouraged migration, metastasis, and proliferation of BxPC-3 cells, and suppression reversed it. We also noticed that thioredoxin-interacting protein (TXNIP) was the potential target of miR-125b. The outcomes also suggested that miR-125b governed the expression of TXNIP inversely via directly attaching to the three prime untranslated region (3'-UTR) activating hypoxia-inducible factor 1α (HIF1α). Looking into the relation between HIF1α and TXNIP, we discovered that TXNIP caused the degradation and export of HIF1α by making a complex with it.The miR-125b-TXNIP-HIF1α pathway may serve as a useful strategy for diagnosing and treating PC.