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Updated: Feb 14, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Androgen receptor reverts dexamethasone‑induced inhibition of prostate cancer cell proliferation and migration
Ju Guo1, Ke Ma2, Hai-Mei Xia3
1Department of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Abstract:
The aim of the present study was to determine the role of androgen receptor in the effect of dexamethasone on cell proliferation and migration of multiple prostate cancer cells. The prostate cancer cell lines LNCaP, 22Rv1, C4‑2 and PC3 were cultured in vitro. For glucocorticoid‑induced experiments, the cells were transferred and cultured in RPMI‑1640 medium with 10% charcoal‑stripped serum from RPMI‑1640 medium with 10% fetal bovine serum for at least 24 h. The effects of dexamethasone on the proliferation and migration of various cell lines were analyzed by MTT and migration assays. Dexamethasone exhibited no effect on LNCaP, C4‑2 and 22Rv1 cell lines, but suppressed proliferation of glucocorticoid receptor (GR)+ androgen receptor (AR)‑ PC3 cell line. Dexamethasone suppressed PC3 cell migration, and did not affect migration of PC3‑AR9 cells. Dexamethasone positively or negatively regulated proliferation of various prostate cancer cells based on AR and GR expression profiles. The data presented in the present study indicates that androgen receptor reverts the dexamethasone‑induced inhibition of prostate cancer cell proliferation and migration.
Insights
Androgen receptor (AR) influences how dexamethasone affects prostate cancer cells. AR can reverse dexamethasone
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Prostate cancer treatment often involves hormonal therapies.
- Glucocorticoids like dexamethasone can impact cancer cell behavior.
- The role of androgen receptor (AR) in mediating these effects is not fully understood.
Purpose of the Study:
- To investigate the role of androgen receptor (AR) in mediating the effects of dexamethasone on prostate cancer cell proliferation and migration.
- To determine how AR and glucocorticoid receptor (GR) expression profiles influence cellular responses to dexamethasone.
Main Methods:
- Utilized multiple prostate cancer cell lines (LNCaP, 22Rv1, C4-2, PC3) in in vitro culture.
- Administered dexamethasone after charcoal-stripping serum to ensure glucocorticoid-specific effects.
- Assessed cell proliferation using MTT assays and cell migration using migration assays.
Main Results:
- Dexamethasone suppressed proliferation and migration in PC3 cells (GR+, AR-).
- No significant effect of dexamethasone was observed on LNCaP, C4-2, and 22Rv1 cell lines.
- Androgen receptor (AR) expression was found to revert dexamethasone-induced inhibition of proliferation and migration.
Conclusions:
- Androgen receptor (AR) plays a critical role in modulating the response of prostate cancer cells to dexamethasone.
- The expression status of both AR and glucocorticoid receptor (GR) dictates whether dexamethasone inhibits or has no effect on cell proliferation and migration.
- AR acts as a key factor in reversing the inhibitory effects of dexamethasone on prostate cancer cell growth and movement.
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