LINC01137 facilitates pancreatic cancer stemness, chemoresistance and proliferation via the miR-7155-5p/KLF12/PI3K-Akt axis.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most prevalent and malignant types of pancreatic cancer, with a 5-year survival rate of approximately 13 %. Cancer stem cells (CSCs) 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. Recent studies have linked lncRNAs to CSCs and chemoresistance. Although LINC01137 was predicted to be associated with pancreatic CSCs (PCSCs), its specific functions and mechanisms in pancreatic cancer remain unclear. In this study, we identified LINC01137 as a PCSC-associated lncRNA that is upregulated in pancreatic cancer tissues and cell lines. High LINC01137 expression correlated with poor prognosis. Knockdown of LINC01137 reduced pancreatic cancer stemness, chemoresistance, and proliferation. Mechanistically, LINC01137 was primarily localized in the cytoplasm and functioned by binding to miR-7155-5p, thereby upregulating KLF12 expression, which in turn activated the PI3K-Akt pathway. Our findings indicate that LINC01137 acts as an oncogene in pancreatic cancer and elucidate its post-transcriptional regulatory mechanisms, suggesting its potential as a therapeutic target.