Objective： To investigate the role of heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) in ferroptosis of pancreatic cancer cells and its potential mechanisms. Methods： Three pancreatic cancer cell lines PaTu8988, MIA-paca2 and PANC1 were treated with different concentrations of Erastin for 3 days. The cell viability was detected by CCK8 method. The half inhibitory concentrations (IC50) of Erastin in three kinds of pancreatic cancer cell lines were calculated and their resistance capabilities to Erastin were compared; qRT-PCR and Western blotting were used to detect the relative expression levels of mRNA and protein of hnRNPA2B1 in pancreatic cancer cells. The differential expression of the hnRNPA2B1 in pancreatic cancer tissues and normal tissues was analyzed by GEPIA, and the survival prognosis of patients with differential expression of hnRNPA2B1 was analyzed from clinical data sets from GEO database. PaTu8988 cells was transfected with sh-Control and sh-hnRNPA2B1 plasmid, respectively, to knock down hnRNPA2B1; PANC1 cells was transfected with Vector and Flag-hnRNPA2B1 plasmid, respectively, to overexpress hnRNPA2B1; and the transfection efficiency was verfied by qRT-PCR and Western blotting, respectively; the effects of knockdown or overexpression of hnRNPA2B1 on the migration and invasion were detected by Transwell assay, and the effects on the proliferation of pancreatic cancer cells were detected by CCK8 assay. The cells in sh-Control, sh-hnRNPA2B1, Vector and Flag-hnRNPA2B1 group were treated with control (0 μmol/L Erastin) and Erastin (IC50 concentration), respectively, then flow cytometry was used to determine the lipid peroxidation level, and colorimetry was used to determine the malindialdehyde (MDA) and tissue iron concentration; in addition to Erastin, the sh-hnRNPA2B1 and Flag-hnRNPA2B1 groups were added with Ferrostatin-1, Necrostatin-1, ZVAD-FMK, respectively, the cells activity was detected by trypan blue dye exclusion. The relative expression levels of RNA and protein of transferrin receptor (TFRC), ferritin heavy chain, glutathione peroxidase 4 and solute carrier family 7 member 11 weredetected by qRT-PCR and Western blotting, respectively. Results： The resistance of three types of pancreatic cancer cells to Erastin from high to low were PaTu8988, MIA-paca2 and PANC1, corresponding Erastin IC50 was 18.020, 15.760 and 2.947 μmol/L, respectively (P<0.05). The relative expression level of hnRNPA2B1 was the highest in PaTu8988 cells, followed by MIA-paca2 cells and the lowest in PANC1 cells (P<0.05), which was the same with Erastin IC50. The expression level of hnRNPA2B1 in pancreatic cancer tissues was significantly higher than that in normol tissues, and the prognosis of patients with higher  expression of hnRNPA2B1 was poor (P<0.05). Down-regulating the expression of hnRNPA2B1, the migration, invasion and proliferation ability of PaTu8988 cells were greatly reduced, while up-regulating was the opposite (P<0-05). Erastin-induced cell death was significantly restored by Ferrostatin-1 not by ZVAD-FMK or Necrostatin-1 (P<0.05); compared with sh-Control group, the level of lipid peroxidation, MDA and iron concentration in sh-hnRNPA2B1 group were significantly increased (P<0.05); compared with Vector group, Flag-hnRNPA2B1 group showed lower level of lipid peroxidation, MDA and ironconcentration (P<0.05). Upregulation of hnRNPA2B1 inhibited the expression of TFRC, while interference with hnRNPA2B1 produced the opposite effect (P<0.05). Conclusion： hnRNPA2B1 could inhibit t he intracelluar accumulation of iron by inhibiting the expression of TFRC, thus promoting the resistance of pancreatic cancer cells to ferroptosis.