EIF3B promotes cancer progression in pancreatic cancer

Background: This study aimed to analyze the relative expression of Eukaryotic Translation Initiation Factor 3 Subunit B (EIF3B) in pancreatic cancer and elucidate its contribution to this disease. Methods: Relative expression of EIF3B in pancreatic cancer was analyzed by immunohistochemistry. Cell viability was determined by the MTT assay and cell proliferation was measured by direct cell counting. Cell apoptosis was detected by Annexin V staining followed by flow cytometry analysis, and cell cycle was analyzed by PI staining. The differential expression gene analysis was performed by microarray. Tumor progression in response to EIF3B deficiency in vivo was investigated using the xenograft tumor model. Results: We found aberrantly high expression of EIF3B in pancreatic cancer, which associated with unfavorable prognosis. Knockdown of EIF3B greatly compromised cell viability and proliferation in both SW1990 and PANC-1 cells. Furthermore, EIF3B deficiency induced cell cycle arrest and spontaneous apoptosis. In vivo tumor progression was significantly suppressed by EIF3B silencing in the xenograft mouse model. Mechanistically, we characterized down-regulation of CDH1 and IRS1 and up-regulation of DDIT3, PTEN and CDKN1B, in response to EIF3B knockdown, which might mediate the oncogenic effect of EIF3B in pancreatic cancer. Conclusions: Our data uncovered the oncogenic role of EIF3B in pancreatic cancer.

Automated summary

This study revealed the oncogenic role of EIF3B in pancreatic cancer, showing aberrantly high expression of EIF3B associated with unfavorable prognosis. Knockdown of EIF3B compromised cell viability and proliferation, inducing cell cycle arrest and spontaneous apoptosis. In vivo tumor progression was significantly suppressed by EIF3B silencing, indicating a potential therapeutic target for pancreatic cancer.