Background:
Pancreatic cancer (PC) is a malignant
tumor with hidden incidence, high degree of
malignancy, rapid
disease progression, and poor prognosis. Eukaryotic
translation initiation factor 3 subunit B (EIF3B) is necessary for
tumor growth, which is an alternative therapeutic target for many
cancers. However, little is known about the relationship between EIF3B and PC. Methods: The expression of EIF3B in PC was detected by immunohistochemistry. EIF3B knockdown cell models were constructed by
lentivirus infection. The MTT assay, the wound-healing assay, the transwell assay, the flow cytometry, and the Human Apoptosis Antibody Array was used to detect the effects of EIF3B knockdown on cell proliferation, cell migration, cell apoptosis, and cell cycle in vitro. Also, the effects of EIF3B knockdown on the
tumor growth of PC were determined in vivo. Results: This study showed that the expression level of EIF3B was significantly up-regulated in PC
tumor tissues and associated with pathological grade. In vitro, EIF3B knockdown inhibited the PC cell proliferation and migration, and the apoptosis levels were obviously promoted by regulating apoptosis-related
proteins including Bcl-2, HSP27, HSP60,
Survivin, sTNF-R2, TNF-α, TNF-β, TRAILR-3, TRAILR-4, and XIAP. Furthermore, the
tumor growth of PC was inhibited after the knockdown of EIF3B in vivo. Conclusion: EIF3B was up-regulated in PC and was a promoter in the development and progression of PC, which could be considered as a therapeutic target for the treatment of PC.