Medical Oncology

, 32:196 | Cite as

The oncogenic role of EIF3D is associated with increased cell cycle progression and motility in prostate cancer

  • Yi Gao
  • Jingfei Teng
  • Yi Hong
  • Fajun Qu
  • Jizhong Ren
  • Lin Li
  • Xiuwu Pan
  • Lu Chen
  • Lei Yin
  • Danfeng XuEmail author
  • Xingang CuiEmail author
Original Paper


EIF3 is the largest multi-protein complex, and several studies have revealed the oncogenic roles of its subunits in many human cancers. However, the roles of EIF3D in the development and progression of PCa remain uncovered. In the present study, the expression of EIF3D in prostate cancer and paracarcinoma tissues, as well as PCa cell lines, was examined. In PCa tissues, the expression of EIF3D was up-regulated compared to that in paracarcinoma tissues. In order to investigate whether EIF3D could serve as potential therapeutic target for prostate cancer, EIF3D was knocked down to verify its functional role in prostate cancer cells. After EIF3D knockdown in PC-3 and DU145 cells, cell proliferation, invasion and colony formation were significantly inhibited; meanwhile, cell cycle analysis revealed cell cycle arrest at G2/M phase. EIF3D is associated with PCa, and silencing EIF3D will result in decreased proliferation, and migration, as well as G2/M arrest in DU145 and PC-3 cells. These results suggest that EIF3D plays an oncogenic role in PCa development and progression.


EIF3D Prostate cancer Oncogenic Cell cycle Mobility 



This work was supported by grants from National Natural Science Foundation of China for Youths (No. 81001136 and 81202020), National Natural Science Foundation of China (No. 30973006, 81170637), Key Project of Science and Innovation Foundation of Shanghai Ministry of Education (14zz084), Shanghai Committee of Science and Technology General Program for Medicine (No. 11JC1402302) and Military Fund for Health Care (13BJZ29).

Conflict of interest

The authors declare that they have no conflict of interest.


  1. 1.
    Siegel R, Naishadham D, Jemal A. Cancer statistics, 2013. Cancer J Clin. 2013;63:11–30.CrossRefGoogle Scholar
  2. 2.
    Visakorpi T. The molecular genetics of prostate cancer. Urology. 2003;62:3–10.PubMedCrossRefGoogle Scholar
  3. 3.
    Dong Z, Zhang JT. Initiation factor eIF3 and regulation of mRNA translation, cell growth, and cancer. Crit Rev Oncol Hematol. 2006;59:169–80.PubMedCrossRefGoogle Scholar
  4. 4.
    Zhang L, Pan X, Hershey JW. Individual overexpression of five subunits of human translation initiation factor eIF3 promotes malignant transformation of immortal fibroblast cells. J Biol Chem. 2007;282:5790–800.PubMedCrossRefGoogle Scholar
  5. 5.
    Shi J, Kahle A, Hershey JW, et al. Decreased expression of eukaryotic initiation factor 3f deregulates translation and apoptosis in tumor cells. Oncogene. 2006;25:4923–36.PubMedCrossRefGoogle Scholar
  6. 6.
    Saramaki O, Willi N, Bratt O, et al. Amplification of EIF3S3 gene is associated with advanced stage in prostate cancer. Am J Pathol. 2001;159:2089–94.PubMedCentralPubMedCrossRefGoogle Scholar
  7. 7.
    Savinainen KJ, Linja MJ, Saramaki OR, et al. Expression and copy number analysis of TRPS1, EIF3S3 and MYC genes in breast and prostate cancer. Br J Cancer. 2004;90:1041–6.PubMedCentralPubMedCrossRefGoogle Scholar
  8. 8.
    Savinainen KJ, Helenius MA, Lehtonen HJ, et al. Overexpression of EIF3S3 promotes cancer cell growth. Prostate. 2006;66:1144–50.PubMedCrossRefGoogle Scholar
  9. 9.
    Johnson LF, Levis R, Abelson HT, et al. Changes in RNA in relation to growth of the fibroblast. IV. Alterations in the production and processing of mRNA and rRNA in resting and growing cells. J Cell Biol. 1976;71:933–8.PubMedCrossRefGoogle Scholar
  10. 10.
    Stanners CP, Adams ME, Harkins JL, et al. Transformed cells have lost control of ribosome number through their growth cycle. J Cell Physiol. 1979;100:127–38.PubMedCrossRefGoogle Scholar
  11. 11.
    Dong Z, Liu Z, Cui P, et al. Role of eIF3a in regulating cell cycle progression. Exp Cell Res. 2009;315:1889–94.PubMedCrossRefGoogle Scholar
  12. 12.
    Dong Z, Liu LH, Han B, et al. Role of eIF3 p170 in controlling synthesis of ribonucleotide reductase M2 and cell growth. Oncogene. 2004;23:3790–801.PubMedCrossRefGoogle Scholar
  13. 13.
    Bachmann F, Banziger R, Burger MM. Cloning of a novel protein overexpressed in human mammary carcinoma. Cancer Res. 1997;57:988–94.PubMedGoogle Scholar
  14. 14.
    Dellas A, Torhorst J, Bachmann F, et al. Expression of p150 in cervical neoplasia and its potential value in predicting survival. Cancer. 1998;83:1376–83.PubMedCrossRefGoogle Scholar
  15. 15.
    Chen G, Burger MM. p150 expression and its prognostic value in squamous-cell carcinoma of the esophagus. Int J Cancer. 1999;84:95–100.PubMedCrossRefGoogle Scholar
  16. 16.
    Pincheira R, Chen Q, Zhang JT. Identification of a 170-kDa protein over-expressed in lung cancers. Br J Cancer. 2001;84:1520–7.PubMedCentralPubMedCrossRefGoogle Scholar
  17. 17.
    Chen G, Burger MM. p150 overexpression in gastric carcinoma: the association with p53, apoptosis and cell proliferation. Int J Cancer. 2004;112:393–8.PubMedCrossRefGoogle Scholar
  18. 18.
    Liang H, Ding X, Zhou C, et al. Knockdown of eukaryotic translation initiation factors 3B (EIF3B) inhibits proliferation and promotes apoptosis in glioblastoma cells. Neurol Sci. 2012;33:1057–62.PubMedCrossRefGoogle Scholar
  19. 19.
    Wang Z, Chen J, Sun J, et al. RNA interference-mediated silencing of eukaryotic translation initiation factor 3, subunit B (EIF3B) gene expression inhibits proliferation of colon cancer cells. World J Surg Oncol. 2012;10:119.PubMedCentralPubMedCrossRefGoogle Scholar
  20. 20.
    Scoles DR, Yong WH, Qin Y, et al. Schwannomin inhibits tumorigenesis through direct interaction with the eukaryotic initiation factor subunit c (eIF3c). Hum Mol Genet. 2006;15:1059–70.PubMedCrossRefGoogle Scholar
  21. 21.
    Rothe M, Ko Y, Albers P, et al. Eukaryotic initiation factor 3 p110 mRNA is overexpressed in testicular seminomas. Am J Pathol. 2000;157:1597–604.PubMedCentralPubMedCrossRefGoogle Scholar
  22. 22.
    Guo Y, Chen JX, Yang S, et al. Selection of reliable reference genes for gene expression study in nasopharyngeal carcinoma. Acta Pharmacol Sin. 2010;31:1487–94.PubMedCentralPubMedCrossRefGoogle Scholar
  23. 23.
    Sudo H, Tsuji AB, Sugyo A, et al. Knockdown of COPA, identified by loss-of-function screen, induces apoptosis and suppresses tumor growth in mesothelioma mouse model. Genomics. 2010;95:210–6.PubMedCrossRefGoogle Scholar
  24. 24.
    Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144:646–74.PubMedCrossRefGoogle Scholar
  25. 25.
    Zhang L, Smit-McBride Z, Pan X, et al. An oncogenic role for the phosphorylated h-subunit of human translation initiation factor eIF3. J Biol Chem. 2008;283:24047–60.PubMedCentralPubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2015

Authors and Affiliations

  • Yi Gao
    • 1
  • Jingfei Teng
    • 3
  • Yi Hong
    • 1
  • Fajun Qu
    • 1
  • Jizhong Ren
    • 1
  • Lin Li
    • 1
  • Xiuwu Pan
    • 1
  • Lu Chen
    • 1
  • Lei Yin
    • 1
  • Danfeng Xu
    • 2
    Email author
  • Xingang Cui
    • 1
    Email author
  1. 1.Department of Urinary Surgery of Changzheng HospitalSecond Military Medical UniversityShanghaiChina
  2. 2.Urology Research Center of PLA, Changzheng HospitalSecond Military Medical UniversityShanghaiChina
  3. 3.General Hospital of Beijing Military CommondBeijingChina

Personalised recommendations