目的 研究RAB2B对胰腺癌细胞生物学行为的影响。 方法 在5株胰腺癌细胞中选出相对高表达RAB2B的PANC-1及相对低表达的BXPC-3细胞，利用细胞转染技术，将RAB2B-siRNA和pcDNA3.1-RAB2B质粒分别转染到PANC-1和BXPC-3细胞。CCK8实验用于检测干预RAB2B后胰腺癌细胞的增殖能力，细胞划痕实验和Transwell小室实验用于检测细胞的迁移和侵袭能力。使用qRT-PCR和蛋白印迹法（WB）分别检测RAB2B、NF-κB、FN1在mRNA及蛋白水平的表达情况。 结果 转染后的PANC-1细胞，其RAB2B的mRNA量及蛋白表达水平均显著下降（P < 0.05）；CCK8结果显示敲低RAB2B后，PANC-1细胞的增殖能力显著降低（P < 0.05），划痕愈合能力明显下降（P < 0.01）；Transwell结果显示细胞迁移数量明显减少（P < 0.01），WB显示磷酸化的p65和FN1的表达量明显下降（P < 0.01）；而过表达RAB2B则逆转了上述改变。 结论 在PANC-1细胞中敲低RAB2B，可以抑制细胞的增殖和迁移能力，而在BXPC-3细胞中过表达RAB2B，可增强细胞的增殖和迁移能力，其机制可能与激活NF-κB通路进而调控FN1的表达有关。

Objective To investigate the effects of Ras?related protein Rab?2B （RAB2B） on the biological behaviors of pancreatic cancer cells and elucidate its underlying mechanism. Methods PANC?1 cells， which exhibit relatively high RAB2B expression， and BXPC?3 cells， which display relatively low RAB2B expression， were selected from five pancreatic cancer cell lines. RAB2B?siRNA and pcDNA3.1?RAB2B plasmids were transfected into PANC?1 and BXPC?3 cells using a cell transfection technique. The CCK?8 assay was employed to evaluate the proliferative capacity of pancreatic cancer cells following RAB2B intervention. Wound healing and Transwell chamber assays were utilized to assess the migratory and invasive capabilities of pancreatic cancer cells. Additionally， the mRNA and protein expression levels of RAB2B， NF?κB， and Fibronectin 1 （FN1） were analyzed by qRT?PCR and Western blot （WB）， respectively. Results RAB2B mRNA and protein expression levels were significantly downregulated in PANC?1 cells following transfection （P < 0.05）. CCK?8 assay results demonstrated that the proliferative capacity of PANC?1 cells was markedly reduced （P < 0.05）， and the wound?healing ability was substantially impaired （P < 0.01） upon RAB2B knockdown. Transwell assays revealed a significant decrease in cell migration （P < 0.01）， while Western blot analysis indicated that the expression levels of phosphorylated p65 and FN1 were notably diminished （P < 0.01）. Conversely， overexpression of RAB2B reversed these aforementioned alterations. Conclusions Knockdown of RAB2B in PANC?1 cells significantly suppresses cell proliferation and migration， whereas overexpression of RAB2B in BXPC?3 cells markedly promotes these processes. This effect is likely mediated through the activation of the NF?κB signaling pathway and the subsequent regulation of FN1 expression.