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. 2021 Nov 10;11(11):1665. doi: 10.3390/biom11111665

Figure 2.

Figure 2

A schematic representation shows that several lncRNAs regulate the PI3K/AKT, MAPK/ERK and JAK2/STAT3 pathways in pancreatic cancer. Growth factor-driven RTK (e.g., EGFR) or cytokine (e.g., IL- 6) signaling can trigger the activation of PI3K/AKT, MAPK/ERK, and JAK2/STAT3 cascades. LncRNAs can affect the activity of these cascades. For instance, HOTAIR can trigger the activation of the JAK2/STAT3 pathway via down-regulating miR-34a expression, thus promoting invasion and migration of pancreatic ductal adenocarcinoma [12]. In addition, GAS5 can up-regulate PTEN expression by down-regulating the expression level of miR-32-5p, therefore inhibiting pancreatic cancer metastasis [41]. LINC01559, through sponging miR-1343-3p, can up-regulate RAF1 expression that can further activate the ERK signaling pathway, thereby enhancing pancreatic cancer progression and metastasis [15]. Green arrows indicate the up-regulation of target genes modulated via lncRNAs; red arrows depict the inhibitory effects.