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Updated: Apr 16, 2026
A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Methylselenocysteine preventing castration-resistant progression of prostate cancer
Yanbo Liu1, Xichun Liu, Yaxiong Guo
1Basic Medical College, Beihua University, Jilin, China; College of Basic Medical Sciences, Jilin University, Changchun, China.
Background:
Castration-resistant progression of prostate cancer after androgen deprivation therapy remains a critical challenge in the clinical management of prostate cancer. Resurgent androgen receptor activity is an established driver of castration-resistant progression, and upregulation of androgen receptor expression has been implicated to contribute to the resurgent androgen receptor activity. We reported previously that methylselenocysteine can decrease the expression and activity of androgen receptor. Here we investigated the ability of methylselenocysteine to inhibit castration-resistant progression of prostate cancer.
Methods:
The regrowth of LNCaP prostate cancer xenografts after castration was monitored. The levels of prostate-specific antigen in mouse serum were measured by ELISA. Tumor cell proliferation and apoptosis were analyzed via Ki-67 immunohistochemistry and TUNEL assay, respectively. Intratumoral angiogenesis was assessed by immunohistochemistry staining of vascular endothelial growth factor and CD31.
Results:
We showed that methylselenocysteine delayed castration-resistant regrowth of LNCaP xenograft tumors after androgen deprivation. This was accompanied by decreased serum levels of prostate-specific antigen, inhibition of prostate cancer cell proliferation and tumor angiogenesis, as well as downregulation of androgen receptor and induction of apoptosis in the relapsed tumors.
Conclusions:
The present study represents the first to show the preclinical efficacy of methylselenocysteine in delaying castration-resistant progression of prostate cancer. The findings provide a rationale for evaluating the clinical application of combining methylselenocysteine with androgen deprivation therapy for the treatment of advanced prostate cancer.
Insights
Methylselenocysteine delays castration-resistant prostate cancer progression by inhibiting tumor growth and angiogenesis. This preclinical study suggests its potential use in combination with androgen deprivation therapy for advanced prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Castration-resistant prostate cancer (CRPC) progression after androgen deprivation therapy (ADT) is a clinical challenge.
- Androgen receptor (AR) activity drives CRPC, with AR expression upregulation contributing to resistance.
- Methylselenocysteine (MSC) previously demonstrated ability to reduce AR expression and activity.
Purpose of the Study:
- To investigate the efficacy of methylselenocysteine in inhibiting CRPC progression.
- To evaluate MSC's impact on CRPC xenograft regrowth and associated biomarkers.
Main Methods:
- Monitoring LNCaP prostate cancer xenograft regrowth post-castration.
- Measuring serum prostate-specific antigen (PSA) via ELISA.
- Analyzing tumor cell proliferation (Ki-67) and apoptosis (TUNEL assay).
- Assessing intratumoral angiogenesis (VEGF, CD31 staining).
Main Results:
- Methylselenocysteine significantly delayed castration-resistant regrowth of LNCaP xenografts.
- MSC treatment led to decreased serum PSA levels.
- Inhibition of prostate cancer cell proliferation and tumor angiogenesis was observed.
- Downregulation of androgen receptor and induction of apoptosis were noted in relapsed tumors.
Conclusions:
- This study provides the first preclinical evidence of methylselenocysteine's efficacy in delaying CRPC progression.
- Findings support further investigation into combining MSC with ADT for advanced prostate cancer treatment.
