Amplification and overexpression of prosaposin in prostate cancer

Shahriar Koochekpour, Yujun Zhang, Rameen Beroukhim, Chia Ling Hsieh, Matthias D. Hofer, Haiyen E. Zhau, Masao Hiraiwa, Daniel Y. Pattan, Joy L. Ware, Ronald B. Luftig, Konrad Sandhoff, Charles L. Sawyers, Kenneth J. Pienta, Mark A. Rubin, Robert L. Vessella, William R. Sellers, Oliver Sartor

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

We identified prosaposin (PSAP) as a secreted protein expressed in androgen-independent (AI) prostate cancer cells by cloning/ sequencing, after probing a PC-3 cDNA library expressed in the λTripIEx phagemid expression vector with a polyclonal rabbit antibody generated against pooled human seminal plasma, PSAP is a neurotrophic molecule; its deficiency or inactivation has proved to be lethal in man and mice, and in mice, it leads to abnormal development and atrophy of the prostate gland, despite normal testosterone levels. We used Southern hybridization, quantitative real-time polymerase chain reaction, and/or single nucleotide polymorphism (SNP) array analysis, and we now report the genomic amplification of PSAP in the metastatic Al prostate cancer cell lines, PC-3, DU-145, MDA-PCa 2b, M-12, and NCI-H660. In addition, by using SNP arrays and a set of 25 punch biopsy samples of human prostate cancer xenografts (LAPC3, LuCaP 23.1, 35, 49, 58, 73, 77, 81, 86.2, 92.1, 93, 96, 105, and 115), lymph nodes, and visceral-organ metastases, we detected amplification of the PSAP locus (10q22.1) in LuCaP 58 and 96 xenografts and two lymph node metastases. In addition, Al metastatic prostate cancer cell lines C4-2B and 1A8-ARCaP over-expressed PSAP mRNA without evidence of genomic amplification. Taken together with prior data that demonstrated the growth-, migration-, and invasion-promoting activities, the activation of multiple signal transduction pathways, and the antiapoptotic effect of PSAP (or one of its active domains, saposin C) in prostate cancer cells, our current observation of PSAP amplification or over-expression in prostate cancer suggests, for the first time, a role for this molecule in the process of carcinogenesis or cancer progression in the prostate.

Original languageEnglish
Pages (from-to)351-364
Number of pages14
JournalGenes Chromosomes and Cancer
Volume44
Issue number4
DOIs
Publication statusPublished - Dec 2005
Externally publishedYes

Fingerprint

Prostatic Neoplasms
Heterografts
Single Nucleotide Polymorphism
Prostate
Saposins
Lymph Nodes
Neoplasm Metastasis
Cell Line
Semen
Gene Library
Androgens
Atrophy
Testosterone
Organism Cloning
Real-Time Polymerase Chain Reaction
Signal Transduction
Carcinogenesis
Observation
Rabbits
Biopsy

ASJC Scopus subject areas

  • Cancer Research
  • Genetics

Cite this

Koochekpour, S., Zhang, Y., Beroukhim, R., Hsieh, C. L., Hofer, M. D., Zhau, H. E., ... Sartor, O. (2005). Amplification and overexpression of prosaposin in prostate cancer. Genes Chromosomes and Cancer, 44(4), 351-364. https://doi.org/10.1002/gcc.20249

Amplification and overexpression of prosaposin in prostate cancer. / Koochekpour, Shahriar; Zhang, Yujun; Beroukhim, Rameen; Hsieh, Chia Ling; Hofer, Matthias D.; Zhau, Haiyen E.; Hiraiwa, Masao; Pattan, Daniel Y.; Ware, Joy L.; Luftig, Ronald B.; Sandhoff, Konrad; Sawyers, Charles L.; Pienta, Kenneth J.; Rubin, Mark A.; Vessella, Robert L.; Sellers, William R.; Sartor, Oliver.

In: Genes Chromosomes and Cancer, Vol. 44, No. 4, 12.2005, p. 351-364.

Research output: Contribution to journalArticle

Koochekpour, S, Zhang, Y, Beroukhim, R, Hsieh, CL, Hofer, MD, Zhau, HE, Hiraiwa, M, Pattan, DY, Ware, JL, Luftig, RB, Sandhoff, K, Sawyers, CL, Pienta, KJ, Rubin, MA, Vessella, RL, Sellers, WR & Sartor, O 2005, 'Amplification and overexpression of prosaposin in prostate cancer', Genes Chromosomes and Cancer, vol. 44, no. 4, pp. 351-364. https://doi.org/10.1002/gcc.20249
Koochekpour, Shahriar ; Zhang, Yujun ; Beroukhim, Rameen ; Hsieh, Chia Ling ; Hofer, Matthias D. ; Zhau, Haiyen E. ; Hiraiwa, Masao ; Pattan, Daniel Y. ; Ware, Joy L. ; Luftig, Ronald B. ; Sandhoff, Konrad ; Sawyers, Charles L. ; Pienta, Kenneth J. ; Rubin, Mark A. ; Vessella, Robert L. ; Sellers, William R. ; Sartor, Oliver. / Amplification and overexpression of prosaposin in prostate cancer. In: Genes Chromosomes and Cancer. 2005 ; Vol. 44, No. 4. pp. 351-364.
@article{eb8b68b68b0c48189ac0e8f453bc9a96,
title = "Amplification and overexpression of prosaposin in prostate cancer",
abstract = "We identified prosaposin (PSAP) as a secreted protein expressed in androgen-independent (AI) prostate cancer cells by cloning/ sequencing, after probing a PC-3 cDNA library expressed in the λTripIEx phagemid expression vector with a polyclonal rabbit antibody generated against pooled human seminal plasma, PSAP is a neurotrophic molecule; its deficiency or inactivation has proved to be lethal in man and mice, and in mice, it leads to abnormal development and atrophy of the prostate gland, despite normal testosterone levels. We used Southern hybridization, quantitative real-time polymerase chain reaction, and/or single nucleotide polymorphism (SNP) array analysis, and we now report the genomic amplification of PSAP in the metastatic Al prostate cancer cell lines, PC-3, DU-145, MDA-PCa 2b, M-12, and NCI-H660. In addition, by using SNP arrays and a set of 25 punch biopsy samples of human prostate cancer xenografts (LAPC3, LuCaP 23.1, 35, 49, 58, 73, 77, 81, 86.2, 92.1, 93, 96, 105, and 115), lymph nodes, and visceral-organ metastases, we detected amplification of the PSAP locus (10q22.1) in LuCaP 58 and 96 xenografts and two lymph node metastases. In addition, Al metastatic prostate cancer cell lines C4-2B and 1A8-ARCaP over-expressed PSAP mRNA without evidence of genomic amplification. Taken together with prior data that demonstrated the growth-, migration-, and invasion-promoting activities, the activation of multiple signal transduction pathways, and the antiapoptotic effect of PSAP (or one of its active domains, saposin C) in prostate cancer cells, our current observation of PSAP amplification or over-expression in prostate cancer suggests, for the first time, a role for this molecule in the process of carcinogenesis or cancer progression in the prostate.",
author = "Shahriar Koochekpour and Yujun Zhang and Rameen Beroukhim and Hsieh, {Chia Ling} and Hofer, {Matthias D.} and Zhau, {Haiyen E.} and Masao Hiraiwa and Pattan, {Daniel Y.} and Ware, {Joy L.} and Luftig, {Ronald B.} and Konrad Sandhoff and Sawyers, {Charles L.} and Pienta, {Kenneth J.} and Rubin, {Mark A.} and Vessella, {Robert L.} and Sellers, {William R.} and Oliver Sartor",
year = "2005",
month = "12",
doi = "10.1002/gcc.20249",
language = "English",
volume = "44",
pages = "351--364",
journal = "Genes Chromosomes and Cancer",
issn = "1045-2257",
publisher = "Wiley-Liss Inc.",
number = "4",

}

TY - JOUR

T1 - Amplification and overexpression of prosaposin in prostate cancer

AU - Koochekpour, Shahriar

AU - Zhang, Yujun

AU - Beroukhim, Rameen

AU - Hsieh, Chia Ling

AU - Hofer, Matthias D.

AU - Zhau, Haiyen E.

AU - Hiraiwa, Masao

AU - Pattan, Daniel Y.

AU - Ware, Joy L.

AU - Luftig, Ronald B.

AU - Sandhoff, Konrad

AU - Sawyers, Charles L.

AU - Pienta, Kenneth J.

AU - Rubin, Mark A.

AU - Vessella, Robert L.

AU - Sellers, William R.

AU - Sartor, Oliver

PY - 2005/12

Y1 - 2005/12

N2 - We identified prosaposin (PSAP) as a secreted protein expressed in androgen-independent (AI) prostate cancer cells by cloning/ sequencing, after probing a PC-3 cDNA library expressed in the λTripIEx phagemid expression vector with a polyclonal rabbit antibody generated against pooled human seminal plasma, PSAP is a neurotrophic molecule; its deficiency or inactivation has proved to be lethal in man and mice, and in mice, it leads to abnormal development and atrophy of the prostate gland, despite normal testosterone levels. We used Southern hybridization, quantitative real-time polymerase chain reaction, and/or single nucleotide polymorphism (SNP) array analysis, and we now report the genomic amplification of PSAP in the metastatic Al prostate cancer cell lines, PC-3, DU-145, MDA-PCa 2b, M-12, and NCI-H660. In addition, by using SNP arrays and a set of 25 punch biopsy samples of human prostate cancer xenografts (LAPC3, LuCaP 23.1, 35, 49, 58, 73, 77, 81, 86.2, 92.1, 93, 96, 105, and 115), lymph nodes, and visceral-organ metastases, we detected amplification of the PSAP locus (10q22.1) in LuCaP 58 and 96 xenografts and two lymph node metastases. In addition, Al metastatic prostate cancer cell lines C4-2B and 1A8-ARCaP over-expressed PSAP mRNA without evidence of genomic amplification. Taken together with prior data that demonstrated the growth-, migration-, and invasion-promoting activities, the activation of multiple signal transduction pathways, and the antiapoptotic effect of PSAP (or one of its active domains, saposin C) in prostate cancer cells, our current observation of PSAP amplification or over-expression in prostate cancer suggests, for the first time, a role for this molecule in the process of carcinogenesis or cancer progression in the prostate.

AB - We identified prosaposin (PSAP) as a secreted protein expressed in androgen-independent (AI) prostate cancer cells by cloning/ sequencing, after probing a PC-3 cDNA library expressed in the λTripIEx phagemid expression vector with a polyclonal rabbit antibody generated against pooled human seminal plasma, PSAP is a neurotrophic molecule; its deficiency or inactivation has proved to be lethal in man and mice, and in mice, it leads to abnormal development and atrophy of the prostate gland, despite normal testosterone levels. We used Southern hybridization, quantitative real-time polymerase chain reaction, and/or single nucleotide polymorphism (SNP) array analysis, and we now report the genomic amplification of PSAP in the metastatic Al prostate cancer cell lines, PC-3, DU-145, MDA-PCa 2b, M-12, and NCI-H660. In addition, by using SNP arrays and a set of 25 punch biopsy samples of human prostate cancer xenografts (LAPC3, LuCaP 23.1, 35, 49, 58, 73, 77, 81, 86.2, 92.1, 93, 96, 105, and 115), lymph nodes, and visceral-organ metastases, we detected amplification of the PSAP locus (10q22.1) in LuCaP 58 and 96 xenografts and two lymph node metastases. In addition, Al metastatic prostate cancer cell lines C4-2B and 1A8-ARCaP over-expressed PSAP mRNA without evidence of genomic amplification. Taken together with prior data that demonstrated the growth-, migration-, and invasion-promoting activities, the activation of multiple signal transduction pathways, and the antiapoptotic effect of PSAP (or one of its active domains, saposin C) in prostate cancer cells, our current observation of PSAP amplification or over-expression in prostate cancer suggests, for the first time, a role for this molecule in the process of carcinogenesis or cancer progression in the prostate.

UR - http://www.scopus.com/inward/record.url?scp=26944466215&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=26944466215&partnerID=8YFLogxK

U2 - 10.1002/gcc.20249

DO - 10.1002/gcc.20249

M3 - Article

C2 - 16080200

AN - SCOPUS:26944466215

VL - 44

SP - 351

EP - 364

JO - Genes Chromosomes and Cancer

JF - Genes Chromosomes and Cancer

SN - 1045-2257

IS - 4

ER -