EIF3B promotes cancer progression in pancreatic cancer

Abstract

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.

Keywords:

• EIF3B
• pancreatic cancer
• cell viability
• apoptosis
• cell cycle

Author contributions

Hanzhang Zhu, Yuqiang Shan, Ke Ge, Jun Lu, Wencheng Kong conducted the experiments and analyzed the data. Hangzhang Zhu and Changku Jia conceived the study. Changku Jia coordinated and supervised the study. Hanzhang Zhu, Yuqiang Shan, Ke Ge, Jun Lu, Wencheng Kong and Changku Jia wrote the manuscript. Hanzhang Zhu, Yuqiang Shan, Ke Ge, Jun Lu, Wencheng Kong and Changku Jia approved the publication of this paper, and are accountable for all aspects of the work and ensure the accuracy or integrity of any part of the work.

Disclosure statement

All authors declare that they have no conflict of interest.

Additional information

Funding

This work was supported by grants from Zhejiang Provincial Natural Science Foundation of China (grant No. LY21H160016) and Medicine and Health Science and Technology Plan Projects of Zhejiang Province (grant No. 2021KY231).