LINC01137 facilitates pancreatic cancer stemness via the miR-7155-5p/KLF12/AKT axis

Abstract Pancreatic cancer, of which pancreatic ductal adenocarcinoma (PDAC) is one of the most prevalent type, is one of the most malignant tumors, with a 5-year survival rate of about 10%. Pancreatic cancer stem cells play pivotal roles in chemoresistance and recurrence. Long non-coding RNAs (lncRNAs) have been identified as key regulators of the biological progression of various cancers. Recently, lncRNAs were found to be associated with cancer stem cells, which are related to chemoresistance. LINC01137 was predicted associated with pancreatic cancer stem cells, however, its function and underlying mechanisms in pancreatic cancer remain unclear. In this study, we found that LINC01137 was upregulated in pancreatic cancer tissues and cell lines. Its high expression correlated with advanced pathological stages and poor prognosis. Induction of LINC01137 expression boosted pancreatic cancer stemness, chemoresistance, and proliferation. Mechanistically, LINC01137 exerted its biological function by binding to miR-7155-5p to activate the KLF12/PI3K/AKT pathway. KLF12 also promoted LINC01137 expression. LINC01137 and KLF12 were involved in promoting PDAC tumorigenesis. Our results suggested that LINC01137 functions as an oncogene in pancreatic cancer and identified its post-transcriptional regulatory mechanisms, which may contribute to targeted therapy for pancreatic cancer.