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Modulation of complement activation by pentraxin-3 in prostate cancer
Giovanni Stallone1,2, Giuseppe Stefano Netti3, Luigi Cormio4
1Nephrology Dialysis and Transplantation Unit, University of Foggia, Viale Luigi Pinto, 251, 71122, Foggia, Italy. giovanni.stallone@unifg.it.
Scientific Reports
|October 28, 2020
Summary
Pentraxin 3 (PTX3) promotes prostate cancer by activating early complement pathways, but not the terminal ones. This immune response is linked to increased cell proliferation and invasion.
Area of Science:
- Immunology
- Oncology
- Urology
Background:
- Pentraxin 3 (PTX3) is an innate immune system component modulating the Complement cascade.
- The Complement system's role in prostate cancer pathogenesis is underappreciated.
- PTX3's specific function in Complement activation during prostate cancer development requires elucidation.
Purpose of the Study:
- To investigate the role of PTX3 in modulating Complement activation during prostate cancer development.
- To analyze the correlation between PTX3 expression, Complement component deposits, and prostate cancer progression.
- To explore the potential pathogenic mechanisms linking PTX3 and prostate cancer.
Main Methods:
- A single-center cohort study involving 620 patients undergoing prostate biopsy.
- Analysis of serum and prostate tissue samples from patients with benign prostatic hyperplasia (BPH) and newly diagnosed prostate cancer.
- Confocal microscopy used to measure PTX3 protein expression and Complement activation (C1q, C3a, C5a receptors, C5b-9, CD59) in tissue samples.
Main Results:
- Increased PTX3 tissue expression was observed in prostate cancer patients (Group A) compared to BPH patients (Group B).
- PTX3 deposits co-localized significantly with C1q deposits in Group A, but were absent in Group B.
- Increased expression of C3a and C5a receptors was found in Group A, with no terminal Complement complex (C5b-9) activation and increased CD59 in cancer tissue.
Conclusions:
- PTX3 plays a significant role in prostate cancer development by recruiting early Complement components.
- The hampered activation of the terminal Complement pathway, coupled with CD59 upregulation, suggests a pro-tumorigenic role for PTX3.
- PTX3 may promote cancer cell proliferation, angiogenesis, and resistance to apoptosis, potentially driving invasion and migration.
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