Abstract
Pancreatic cancer is a malignancy with a poor prognosis and high mortality. The lincRNA TMPOP2 is highly expressed in gynecological cancers and may exhibit tumor-promoting functions. However, the function of TMPOP2 in pancreatic cancer is limited. TMPOP2 expression in pancreatic cancer and adjacent tissues is analyzed from The Cancer Genome Atlas (TCGA) and GTEx database. It shows the high expression of TMPOP2 in pancreatic cancer tissues. Similar results are observed in resected pancreatic adenocarcinoma tumors and adjacent tissues from 20 patients and the relative cell lines. When the pancreatic cell lines are transfected with si-TMPOP2, it shows that TMPOP2 downregulation inhibits the cells migration and EMT. Furthermore, the potential mechanism is explored by detecting the expression of c-Jun N-terminal kinase (JNK), phosphorylated JNK, signal transducer and activator of transcription 3 (STAT3), and phosphorylated STAT3. It suggests that TMPOP2 knockdown inactivates JNK and STAT3 phosphorylation. When a JNK activator (anisomycin) is added to the cells with si-NC or si-TMPOP2, it can partially reverse the migration and EMT inhibition of the cells with inhibited TMPOP2. TMPOP2 inhibition suppresses the migration and EMT of pancreatic cancer by repressing the JNK/STAT3 pathway. Thus, this may be a novel target for pancreatic cancer therapy.