» Articles » PMID: 21189143

Co-expression and Impact of Prostate Specific Membrane Antigen and Prostate Specific Antigen in Prostatic Pathologies

Overview
Publisher Biomed Central
Specialty Oncology
Date 2010 Dec 30
PMID 21189143
Citations 19
Authors
Affiliations
Soon will be listed here.
Abstract

Background: The present study was undertaken to relate the co-expression of prostate-associated antigens, PSMA and PSA, with the degree of vascularization in normal and pathologic (hyperplasia and cancer) prostate tissues to elucidate their possible role in tumor progression.

Methods: The study was carried out in 6 normal, 44 benign prostatic hyperplastic and 39 cancerous human prostates. Immunohistochemical analysis were performed using the monoclonal antibody CD34 to determine the angiogenic activity, and the monoclonal antibodies 3E6 and ER-PR8 to assess PSMA and PSA expression, respectively.

Results: In our study we found that in normal prostate tissue, PSMA and PSA were equally expressed (3.7 ± 0.18 and 3.07 ± 0.11). A significant difference in their expression was see in hyperplastic and neoplastic prostates tissues (16.14 ± 0.17 and 30.72 ± 0.85, respectively) for PSMA and (34.39 ± 0.53 and 17.85 ± 1.21, respectively) for PSA. Study of prostate tumor profiles showed that the profile (PSA+, PSMA-) expression levels decreased between normal prostate, benign prostatic tissue and primary prostate cancer. In the other hand, the profile (PSA-, PSMA+) expression levels increased from normal to prostate tumor tissues. PSMA overexpression was associated with high intratumoral angiogenesis activity. By contrast, high PSA expression was associated with low angiogenesis activity.

Conclusion: These data suggest that these markers are regulated differentially and the difference in their expression showed a correlation with malignant transformation. With regard to the duality PSMA-PSA, this implies the significance of their investigation together in normal and pathologic prostate tissues.

Citing Articles

Rapamycin and Low-dose IL-2 Mediate an Immunosuppressive Microenvironment to Inhibit Benign Prostatic Hyperplasia.

Cao T, Xie F, Shi Y, Xu J, Liu Y, Cui D Int J Biol Sci. 2023; 19(11):3441-3455.

PMID: 37497009 PMC: 10367549. DOI: 10.7150/ijbs.85089.


The Transcriptomic Profiles of and Stratify the Risk of Biochemical Recurrence in Primary Prostate Cancer beyond Clinical Features.

Olczak M, Orzechowska M, Bednarek A, Lipinski M Int J Mol Sci. 2023; 24(9).

PMID: 37176106 PMC: 10179071. DOI: 10.3390/ijms24098399.


Characterization of the Tumor Microenvironment and the Biological Processes with a Role in Prostatic Tumorigenesis.

Ionescu C, Aschie M, Matei E, Cozaru G, Deacu M, Mitroi A Biomedicines. 2022; 10(7).

PMID: 35884977 PMC: 9313300. DOI: 10.3390/biomedicines10071672.


KLK3 in the Regulation of Angiogenesis-Tumorigenic or Not?.

Koistinen H, Kunnapuu J, Jeltsch M Int J Mol Sci. 2021; 22(24).

PMID: 34948344 PMC: 8704207. DOI: 10.3390/ijms222413545.


Molecular Imaging in Primary Staging of Prostate Cancer Patients: Current Aspects and Future Trends.

Manafi-Farid R, Ranjbar S, Jamshidi Araghi Z, Pilz J, Schweighofer-Zwink G, Pirich C Cancers (Basel). 2021; 13(21).

PMID: 34771523 PMC: 8582501. DOI: 10.3390/cancers13215360.


References
1.
Wright Jr G, Grob B, Haley C, Grossman K, Newhall K, Petrylak D . Upregulation of prostate-specific membrane antigen after androgen-deprivation therapy. Urology. 1996; 48(2):326-34. DOI: 10.1016/s0090-4295(96)00184-7. View

2.
Stege R, Grande M, Carlstrom K, Tribukait B, Pousette A . Prognostic significance of tissue prostate-specific antigen in endocrine-treated prostate carcinomas. Clin Cancer Res. 2000; 6(1):160-5. View

3.
Denmeade S, Sokoll L, Dalrymple S, Rosen D, Gady A, Bruzek D . Dissociation between androgen responsiveness for malignant growth vs. expression of prostate specific differentiation markers PSA, hK2, and PSMA in human prostate cancer models. Prostate. 2003; 54(4):249-57. DOI: 10.1002/pros.10199. View

4.
Israeli R, Powell C, Fair W, Heston W . Molecular cloning of a complementary DNA encoding a prostate-specific membrane antigen. Cancer Res. 1993; 53(2):227-30. View

5.
Puhr M, Santer F, Neuwirt H, Marcias G, Hobisch A, Culig Z . SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling. Endocr Relat Cancer. 2010; 17(2):525-38. DOI: 10.1677/ERC-10-0007. View