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Generation of Prostate Cancer Patient Derived Xenograft Models from Circulating Tumor Cells
Published on: October 20, 2015
The induction of Maspin expression by a glucosamine-derivative has an antiproliferative activity in prostate cancer
Rossana Cocchiola1, Mariangela Lopreiato1, Raffaella Guazzo2
1Dept. of Biochemical Sciences, Sapienza University of Roma, P.le Aldo Moro, 5, 00185, Roma, Italy.
Abstract:
Mammary serine protease inhibitor or Maspin has been characterized as a class II tumor suppressor gene in several cancer types, among them prostate cancer (CaP). Androgen ablation is an effective therapy for CaP, but with short-term effectiveness, thus new therapeutic strategies are actively sought. The present study is aimed to explore the effects of a glucosamine derivative, 2-(N-Carbobenzyloxy)l-phenylalanylamido-2-deoxy-β-d-glucose (NCPA), on two CaP cell lines, PC3 and LNCaP. In particular we analyzed the impact of NCPA on Maspin production, cell viability and cell cycle progression and apoptosis/necrosis pathway activation in PC3 and LNCaP cell lines. NCPA is able to stimulate Maspin production in PC3 and not in LNCaP cell lines. NCPA blocks the PC3 cell cycle in G1 phase, by inhibiting Cyclin D1 production and induces the apoptosis, therefore interfering with aggressiveness of this androgen-insensitive cell line. Moreover, NCPA is able to induce the expression of Maspin in LNCaP cell line treated with androgen receptor inhibitor, Bicalutamide, and in turn to stimulate the apoptosis of these cells. These findings suggest that NCPA, stimulating the endogenous production of a tumor suppressor protein, could be useful in the design of new therapeutic strategies for treatment of CaP.
Insights
A novel glucosamine derivative, NCPA, shows promise for prostate cancer (CaP) treatment by boosting the tumor suppressor Maspin. It inhibits cancer cell growth and promotes apoptosis in both androgen-sensitive and insensitive CaP cell lines.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Maspin is a tumor suppressor gene implicated in prostate cancer (CaP).
- Current therapies like androgen ablation offer limited long-term effectiveness for CaP.
- Novel therapeutic strategies targeting CaP progression are urgently needed.
Purpose of the Study:
- To investigate the effects of a glucosamine derivative, NCPA, on prostate cancer cell lines.
- To analyze NCPA's impact on Maspin production, cell viability, cell cycle, and apoptosis/necrosis pathways.
- To explore NCPA's potential as a therapeutic agent for CaP.
Main Methods:
- Treatment of PC3 and LNCaP prostate cancer cell lines with NCPA.
- Analysis of Maspin production levels.
- Assessment of cell viability, cell cycle progression (G1 phase, Cyclin D1), and apoptosis/necrosis.
- Evaluation of NCPA effects in combination with Bicalutamide in LNCaP cells.
Main Results:
- NCPA stimulated Maspin production in PC3 cells but not LNCaP cells.
- NCPA inhibited PC3 cell cycle progression at the G1 phase by reducing Cyclin D1 and induced apoptosis.
- NCPA induced Maspin expression and apoptosis in Bicalutamide-treated LNCaP cells.
Conclusions:
- NCPA demonstrates potential as a therapeutic agent for prostate cancer by stimulating Maspin production.
- NCPA exhibits anti-cancer effects by inhibiting cell cycle progression and inducing apoptosis in CaP cells.
- NCPA could be valuable in developing new therapeutic strategies for CaP, including androgen-insensitive forms.
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