Encyclopedia of Signaling Molecules

2018 Edition
| Editors: Sangdun Choi

Tumor Protein D52 (TPD52)

  • Yuyan Chen
  • Jennifer A. ByrneEmail author
Reference work entry
DOI: https://doi.org/10.1007/978-3-319-67199-4_101930


Historical Background

Mammalian TPD52 sequences were first described in the mid-1990s, through a number of independent reports and experimental approaches. Publications from 1995 to 1996 identified TPD52 sequences through the detection of increased TPD52 transcript levels in human cancer tissue or cell lines, relative to nonmalignant controls. Orthologous rat, rabbit, or quail transcripts were identified as either encoding proteins that are phosphorylated in response to raised intracellular calcium levels or as a retroviral target gene, respectively. Early reports also identified paralogous human and mouse transcript sequences, and these reports, combined with genome sequencing, demonstrated that TPD52 is one gene within a four-member gene family (reviewed by Boutros et al. 2004; Byrne et al. 2014). While TPD52-like protein sequences are...

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  1. Boutros R, Fanayan S, Shehata M, Byrne JA. The tumor protein D52 family: many pieces, many puzzles. Biochem Biophys Res Commun. 2004;325:1115–21.PubMedPubMedCentralCrossRefGoogle Scholar
  2. Byrne JA, Frost S, Chen Y, Bright RK. Tumor protein D52 (TPD52) and cancer-oncogene understudy or understudied oncogene? Tumour Biol. 2014;35:7369–82. doi:10.1007/s13277-014-2006-x.CrossRefPubMedPubMedCentralGoogle Scholar
  3. Chen Y, Kamili A, Hardy JR, Groblewski GE, Khanna KK, Byrne JA. Tumor protein D52 represents a negative regulator of ATM protein levels. Cell Cycle. 2013;12:3083–97. doi:10.4161/cc.26146.CrossRefPubMedPubMedCentralGoogle Scholar
  4. Dawson SJ, Rueda OM, Aparicio S, Caldas C. A new genome-driven integrated classification of breast cancer and its implications. EMBO J. 2013;32:617–28. doi:10.1038/emboj.2013.19.CrossRefPubMedPubMedCentralGoogle Scholar
  5. Donzelli S, Mori F, Bellissimo T, Sacconi A, Casini B, Frixa T, et al. Epigenetic silencing of miR-145-5p contributes to brain metastasis. Oncotarget. 2015;6:35183–201. doi:10.18632/oncotarget.5930.CrossRefPubMedPubMedCentralGoogle Scholar
  6. Goto Y, Nishikawa R, Kojima S, Chiyomaru T, Enokida H, Inoguchi S, et al. Tumour-suppressive microRNA-224 inhibits cancer cell migration and invasion via targeting oncogenic TPD52 in prostate cancer. FEBS Lett. 2014;588:1973–82. doi:10.1016/j.febslet.2014.04.020.CrossRefPubMedPubMedCentralGoogle Scholar
  7. Han G, Fan M, Zhang X. microRNA-218 inhibits prostate cancer cell growth and promotes apoptosis by repressing TPD52 expression. Biochem Biophys Res Commun. 2015;456:804–9. doi:10.1016/j.bbrc.2014.12.026.CrossRefPubMedPubMedCentralGoogle Scholar
  8. Kamili A, Roslan N, Frost S, Cantrill LC, Wang D, Della-Franca A, et al. TPD52 expression increases neutral lipid storage within cultured cells. J Cell Sci. 2015;128:3223–38.PubMedPubMedCentralCrossRefGoogle Scholar
  9. Kumamoto T, Seki N, Mataki H, Mizuno K, Kamikawaji K, Samukawa T, et al. Regulation of TPD52 by antitumor microRNA-218 suppresses cancer cell migration and invasion in lung squamous cell carcinoma. Int J Oncol. 2016;49:1870–80. doi:10.3892/ijo.2016.3690.CrossRefPubMedPubMedCentralGoogle Scholar
  10. Li G, Yao L, Zhang J, Li X, Dang S, Zeng K, et al. Tumor-suppressive microRNA-34a inhibits breast cancer cell migration and invasion via targeting oncogenic TPD52. Tumour Biol. 2016;37:7481–91. doi:10.1007/s13277-015-4623-4.CrossRefPubMedPubMedCentralGoogle Scholar
  11. Marcotte R, Sayad A, Brown KR, Sanchez-Garcia F, Reimand J, Haider M, et al. Functional genomic landscape of human breast cancer drivers, vulnerabilities, and resistance. Cell. 2016;164:293–309. doi:10.1016/j.cell.2015.11.062.CrossRefPubMedPubMedCentralGoogle Scholar
  12. Mataki H, Seki N, Mizuno K, Nohata N, Kamikawaji K, Kumamoto T, et al. Dual-strand tumor-suppressor microRNA-145 (miR-145-5p and miR-145-3p) coordinately targeted MTDH in lung squamous cell carcinoma. Oncotarget. 2016;7:72084–98. doi: 10.18632/oncotarget.12290.Google Scholar
  13. Moritz T, Venz S, Junker H, Kreuz S, Walther R, Zimmermann U. Isoform 1 of TPD52 (PC-1) promotes neuroendocrine transdifferentiation in prostate cancer cells. Tumour Biol. 2016;37:10435–46. doi:10.1007/s13277-016-4925-1.CrossRefPubMedPubMedCentralGoogle Scholar
  14. Okato A, Goto Y, Kurozumi A, Kato M, Kojima S, Matsushita R, et al. Direct regulation of LAMP1 by tumor-suppressive microRNA-320a in prostate cancer. Int J Oncol. 2016;49:111–22. doi:10.3892/ijo.2016.3522.CrossRefPubMedPubMedCentralGoogle Scholar
  15. Ross-Adams H, Lamb AD, Dunning MJ, Halim S, Lindberg J, Massie CM, et al. Integration of copy number and transcriptomics provides risk stratification in prostate cancer: a discovery and validation cohort study. EBioMedicine. 2015;2:1133–44. doi:10.1016/j.ebiom.2015.07.017.CrossRefPubMedPubMedCentralGoogle Scholar
  16. Shang ZF, Wei Q, Yu L, Huang F, Xiao BB, Wang H, et al. Suppression of PC-1/PrLZ sensitizes prostate cancer cells to ionizing radiation by attenuating DNA damage repair and inducing autophagic cell death. Oncotarget. 2016;7:62340–51. doi:10.18632/oncotarget.11470.CrossRefPubMedPubMedCentralGoogle Scholar
  17. Shehata M, Weidenhofer J, Thamotharampillai K, Hardy JR, Byrne JA. Tumor protein D52 overexpression and gene amplification in cancers from a mosaic of microarrays. Crit Rev Oncog. 2008;14:33–55.PubMedPubMedCentralCrossRefGoogle Scholar
  18. Wang J, Zhang H, Zhang X, Wang P, Wang H, Huang F, et al. PC-1 works in conjunction with E3 ligase CHIP to regulate androgen receptor stability and activity. Oncotarget. 2016;7:81377–88. doi: 10.18632/oncotarget.13230.Google Scholar
  19. Wu R, Wang H, Wang J, Wang P, Huang F, Xie B, et al. EphA3, induced by PC-1/PrLZ, contributes to the malignant progression of prostate cancer. Oncol Rep. 2014;32:2657–65. doi:10.3892/or.2014.3482.CrossRefPubMedPubMedCentralGoogle Scholar
  20. Yu L, Shang ZF, Wang J, Wang H, Huang F, Zhang Z, et al. PC-1/PrLZ confers resistance to rapamycin in prostate cancer cells through increased 4E-BP1 stability. Oncotarget. 2015;6:20356–69.PubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing AG 2018

Authors and Affiliations

  1. 1.Molecular Oncology Laboratory, Children’s Cancer Research Unit, Kids Research InstituteThe Children‘s Hospital at WestmeadWestmeadAustralia