Pancreatic cancer (PC) is a malignant cancer with high mortality and poor prognosis. In this study, we found that Linc01232 was significantly upregulated in PC tissues and cells and higher Linc01232 expression was associated with poorer prognosis. Linc01232 overexpression promoted and Linc01232 knockdown inhibited the migration and invasion of PC cells. The results of RNA pull-down, RNA Binding Protein Immunoprecipitation (RIP) assays revealed that Linc01232 physically interacted with Heterogeneous Nuclear Ribonucleoprotein A2/B1 (HNRNPA2B1) (680–890 nt fragment with the RNA recognition motif 2 domain) to inhibit its ubiquitin-mediated degradation in PC cells. RNA sequencing was performed to obtain the transcriptional profiles regulated by Linc01232 and we further demonstrated that Linc01232 participated in the alternative splicing of A-Raf by stabilizing HNRNPA2B1 and subsequently regulated the MAPK/ERK signaling pathway. Collected, our study showed that Linc01232/HNRNPA2B1/A-Raf/MAPK axis participated in the progression of PC and provided a potential therapeutic target for PC.

胰腺癌（PC）是一种死亡率高，预后差的恶性肿瘤。在这项研究中，我们发现Linc01232在PC组织和细胞中显着上调，而较高的Linc01232表达与较差的预后相关。Linc01232的过度表达得到促进，Linc01232的敲低抑制了PC细胞的迁移和侵袭。RNA下拉，RNA结合蛋白免疫沉淀（RIP）分析的结果表明，Linc01232与异质核核糖蛋白A2 / B1（HNRNPA2B1）（具有RNA识别基序2结构域的680-890 nt片段）发生物理相互作用，从而抑制了其遍在蛋白-介导的PC细胞降解。进行RNA测序以获得由Linc01232调控的转录谱，我们进一步证明Linc01232通过稳定HNRNPA2B1参与了A-Raf的选择性剪接，并随后调控了MAPK / ERK信号通路。收集后，我们的研究表明Linc01232 / HNRNPA2B1 / A-Raf / MAPK轴参与了PC的发展，并为PC提供了潜在的治疗靶点。