Identification of the deleted in split hand/split foot 1 protein as a novel biomarker for human cervical cancer

Carcinogenesis

Volumn 34, Issue 1, 2013, Pages 68-78

  Ma, Yen Ying ^a   Lin, Hao ^a   Chang, Fang Mei ^b   Chang, Ting Chang ^a   Trieu, Tiffany ^b   Pridgen, Hannah I ^b   Zhang, Yinghao ^b   Huang, Jianjun ^b,c   Patĩo guzman, Karina ^b   Diab, Nabih ^b   Cantu, Angelica ^b   Slaga, Thomas J ^b   Wei, Sung Jen ^b  

^a CHANG GUNG UNIVERSITY COLLEGE OF MEDICINE   (Taiwan)

^b University of Texas Health Science Center   (United States)

^c Central South University   (China)

Author keywords

[No Author keywords available]

Indexed keywords

ACID PROTEIN; CASPASE 3; CISPLATIN; DELETED IN SPLIT HAND SPLIT FOOT 1 PROTEIN; MESSENGER RNA; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; PROTEIN P53; SHORT HAIRPIN RNA; TUMOR MARKER; UNCLASSIFIED DRUG;

APOPTOSIS; ARTICLE; CANCER CELL CULTURE; CANCER DIAGNOSIS; CANCER GRADING; CELL DEATH; CYTOTOXICITY; EARLY DIAGNOSIS; GENE EXPRESSION; GENE SILENCING; HELA CELL; HUMAN; HUMAN CELL; HUMAN CELL CULTURE; HUMAN TISSUE; LYMPH NODE METASTASIS; MALIGNANT TRANSFORMATION; PRIORITY JOURNAL; PROTEIN ANALYSIS; PROTEIN EXPRESSION; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; TUMOR VOLUME; UTERINE CERVIX CANCER; UTERINE CERVIX EPITHELIUM;

BASE SEQUENCE; DNA PRIMERS; FEMALE; GENE KNOCKDOWN TECHNIQUES; HUMANS; POLYMERASE CHAIN REACTION; PROTEASOME ENDOPEPTIDASE COMPLEX; RNA, MESSENGER; TUMOR MARKERS, BIOLOGICAL; UTERINE CERVICAL NEOPLASMS;

EID: 84872135042     PISSN: 01433334     EISSN: 14602180     Source Type: Journal    
DOI: 10.1093/carcin/bgs279     Document Type: Article

References (44)

1. Shah,K.V. et al. (1996) In: Fields, B.N. et al. (ed.) Fields Virology. Lippincott-Raven Publishers, Philadelphia.
2. World Health Organization. (2011) WHO/ICO Information Centre on Human Papilloma Virus and Cervical Cancer. http://www.who.int/hpvcentre/ statistics/en/ (2 April 2011, date last accessed).
3. Schiffman,M.H. et al. (1993) Epidemiologic evidence showing that human papillomavirus infection causes most cervical intraepithelial neoplasia. J. Natl. Cancer Inst., 85, 958-964.
4. zur Hausen,H. (1994) Molecular pathogenesis of cancer of the cervix and its causation by specific human papillomavirus. In zur Hausen, H. (ed.) Human Pathogenic Papillomavirus. Springer-Verlag, Berlin, pp. 131-156.
5. von Knebel Doeberitz,M. et al. (1988) Correlation of modified human papilloma virus early gene expression with altered growth properties in C4-1 cervical carcinoma cells. Cancer Res., 48, 3780-3786.
6. Ueda,Y. et al. (2003) Monoclonal expansion with integration of highrisk type human papillomaviruses is an initial step for cervical carcinogenesis: association of clonal status and human papillomavirus infection with clinical outcome in cervical intraepithelial neoplasia. Lab. Invest., 83, 1517-1527.
7. Werness,B.A. et al. (1990) Association of human papillomavirus types 16 and 18 E6 proteins with p53. Science (Washington DC), 248, 76-79.
8. Dyson,N. et al. (1989) The human papilloma virus 16 E7 oncoprotein is able to bind the retinoblastoma gene product. Science (Washington DC), 243, 934-936.
9. Ma,Y.Y. et al. (2000) PIK3CA as an oncogene in cervical cancer. Oncogene, 19, 2739-2744.
10. Kennedy,S.G. et al. (1997) The PI 3-kinase/Akt signaling pathway delivers an anti-apoptotic signal. Genes Dev., 11, 701-713.
11. Marte,B.M. et al. (1997) PKB/Akt: connecting phosphoinositide 3-kinase to cell survival and beyond. Trends Biochem. Sci., 22, 355-358.
12. Crackower,M.A. et al. (1996) Characterization of the split hand/split foot malformation locus SHFM1 at 7q21.3-q22.1 and analysis of a candidate gene for its expression during limb development. Hum. Mol. Genet., 5, 571-579.
13. Jäntti,J. et al. (1999) SEM1, a homologue of the split hand/split foot malformation candidate gene Dss1, regulates exocytosis and pseudohyphal differentiation in yeast. Proc. Natl. Acad. Sci. U.S.A., 96, 909-914.
14. Marston,N.J. et al. (1999) Interaction between the product of the breast cancer susceptibility gene BRCA2 and DSS1, a protein functionally conserved from yeast to mammals. Mol. Cell. Biol., 19, 4633-4642.
15. Gudmundsdottir,K. et al. (2004) DSS1 is required for RAD51 focus formation and genomic stability in mammalian cells. EMBO Rep., 5, 1-5.
16. Li,J. et al. (2006) DSS1 is required for the stability of BRCA2. Oncogene, 25, 1186-1194.
17. Yang,H. et al. (2002) BRCA2 function in DNA binding and recombination from a BRCA2-DSS1-ssDNA structure. Science, 297, 1837-1848.
18. Kojic,M. et al. (2003) The BRCA2-interacting protein DSS1 is vital for DNA repair, recombination, and genome stability in Ustilago maydis. Mol. Cell, 12, 1043-1049.
19. Kojic,M. et al. (2005) Brh2-Dss1 interplay enables properly controlled recombination in Ustilago maydis. Mol. Cell. Biol., 25, 2547-2557.
20. Krogan,N.J. et al. (2004) Proteasome involvement in the repair of DNA double-strand breaks. Mol. Cell, 16, 1027-1034.
21. Zhou,Q. et al. (2007) Dss1 interaction with Brh2 as a regulatory mechanism for recombinational repair. Mol. Cell. Biol., 27, 2512-2526.
22. Wei,S.J. et al. (2003) Identification of Dss1 as a 12-O-tetradecanoylphorbol-13-acetate-responsive gene expressed in keratinocyte progenitor cells, with possible involvement in early skin tumorigenesis. J. Biol. Chem., 278, 1758-1768.
23. Funakoshi,M. et al. (2004) Sem1, the yeast ortholog of a human BRCA2-binding protein, is a component of the proteasome regulatory particle that enhances proteasome stability. J. Cell. Sci., 117(Pt 26), 6447-6454.
24. Sone,T. et al. (2004) Sem1p is a novel subunit of the 26 S proteasome from Saccharomyces cerevisiae. J. Biol. Chem., 279, 28807-28816.
25. Wei,S.J. et al. (2008) Identification of a specific motif of the DSS1 protein required for proteasome interaction and p53 protein degradation. J. Mol. Biol., 383, 693-712.
26. Thakurta,A.G. et al. (2005) Homolog of BRCA2-interacting Dss1p and Uap56p link Mlo3p and Rae1p for mRNA export in fission yeast. EMBO J., 24, 2512-2523.
27. Lin,H. et al. (2005) A simple method for the detection and genotyping of high-risk human papillomavirus using seminested polymerase chain reaction and reverse hybridization. Gynecol. Oncol., 96, 84-91.
28. Cox,A.D. et al. (1994) Biological assays for cellular transformation. Meth. Enzymol., 238, 277-294.
29. Wei,S.J. et al. (2004) 12-O-tetradecanoylphorbol-13-acetate and UV radiation-induced nucleoside diphosphate protein kinase B mediates neoplastic transformation of epidermal cells. J. Biol. Chem., 279, 5993-6004.
30. Wei,S.J. et al. (1998) S- and G2-phase cell cycle arrests and apoptosis induced by ganciclovir in murine melanoma cells transduced with herpes simplex virus thymidine kinase. Exp. Cell Res., 241, 66-75.
31. Kononen,J. et al. (1998) Tissue microarrays for high-throughput molecular profiling of tumor specimens. Nat. Med., 4, 844-847.
32. Rundhaug,J.E. et al. (2005) SAGE profiling of UV-induced mouse skin squamous cell carcinomas, comparison with acute UV irradiation effects. Mol. Carcinog., 42, 40-52.
33. Kamelle,S.A. et al. (2004) Surgical-pathological predictors of disease-free survival and risk groupings for IB2 cervical cancer: do the traditional models still apply? Gynecol. Oncol., 94, 249-255.
34. Marchiolé,P. et al. (2005) Clinical significance of lympho vascular space involvement and lymph node micrometastases in early-stage cervical cancer: a retrospective case-control surgico-pathological study. Gynecol. Oncol., 97, 727-732.
35. Creasman,W.T. et al. (2004) Is lymph vascular space involvement an independent prognostic factor in early cervical cancer? Gynecol. Oncol., 92, 525-529.
36. Ho,C.M. et al. (2004) Multivariate analysis of the prognostic factors and outcomes in early cervical cancer patients undergoing radical hysterectomy. Gynecol. Oncol., 93, 458-464.
37. Delgado,G. et al. (1990) Prospective surgical-pathological study of disease-free interval in patients with stage IB squamous cell carcinoma of the cervix: a Gynecologic Oncology Group study. Gynecol. Oncol., 38, 352-357.
38. Averette,H.E. et al. (1993) Radical hysterectomy for invasive cervical cancer. A 25-year prospective experience with the Miami technique. Cancer, 71(4 Suppl), 1422-1437.
39. Sasagawa,T. et al. (1992) Induction of uterine cervical neoplasias in mice by human papillomavirus type 16 E6/E7 genes. Cancer Res., 52, 4420-4426.
40. Lin,Z. et al. (2009) Combination of proteasome and HDAC inhibitors for uterine cervical cancer treatment. Clin. Cancer Res., 15, 570-577.
41. Hougardy,B.M. et al. (2006) Proteasome inhibitor MG132 sensitizes HPVpositive human cervical cancer cells to rhTRAIL-induced apoptosis. Int. J. Cancer, 118, 1892-1900.
42. Yamato,K. et al. (2006) Induction of cell death in human papillomavirus 18-positive cervical cancer cells by E6 siRNA. Cancer Gene Ther., 13, 234-241.
43. Yamato,K. et al. (2008) New highly potent and specific E6 and E7 siRNAs for treatment of HPV16 positive cervical cancer. Cancer Gene Ther., 15, 140-153.
44. Tan, S. et al. (2012) HPV16 E6 RNA interference enhances cisplatin and death receptor mediated apoptosis in human cervical carcinoma cells. Mol. Pharmacol., 81, 701-709.