RhoGDIα suppresses growth and survival of prostate cancer cells

Yezi Zhu, Ramakumar Tummala, Chengfei Liu, Nagalakshmi Nadiminty, Wei Lou, Christopher P Evans, Qinghua Zhou, Allen C Gao

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

BACKGROUND Treatment for primary prostate cancer (CaP) is the withdrawal of androgens. However, CaP eventually progresses to grow in a castration-resistant state. The mechanisms involved in the development and progression of castration-resistant prostate cancer (CRPC) remain unknown. We have previously generated LNCaP-IL6+ cells by treating LNCaP cells chronically with interleukin-6 (IL-6), which have acquired the ability to grow in androgen-deprived conditions. METHODS We compared the protein expression profile of LNCaP and LNCaP-IL6+ cells using two-dimensional gel electrophoresis. The gels were then silver stained in order to visualize proteins and the differentially expressed spots were identified and characterized by micro sequencing using MALDI-PMF mass spectrometry. RESULTS In this study, we have identified RhoGDIα (GDIα) as a suppressor of CaP growth. Expression of GDIα was reduced in LNCaP-IL6+ cells and was down-regulated in more aggressive CaP cells compared to LNCaP cells. Over expression of GDIα inhibited the growth of CaP cells and caused LNCaP-IL6+ cells reversal to androgen-sensitive state, while down-regulation of GDIα enhanced growth of androgen-sensitive LNCaP CaP cells in androgen-deprived conditions. In addition, GDIα suppressed the tumorigenic ability of prostate tumor xenografts in vivo. CONCLUSIONS These results demonstrate that loss of GDIα expression promotes the development and progression of prostate cancer.

Original languageEnglish (US)
Pages (from-to)392-398
Number of pages7
JournalProstate
Volume72
Issue number4
DOIs
StatePublished - Mar 2012

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Guanine Nucleotide Dissociation Inhibitors
Prostatic Neoplasms
Growth
Androgens
Interleukin-6
Castration
Matrix-Assisted Laser Desorption-Ionization Mass Spectrometry
Electrophoresis, Gel, Two-Dimensional
Silver
Heterografts
Prostate
Mass Spectrometry
Proteins
Down-Regulation
Gels

Keywords

  • IL-6
  • prostate cancer
  • RhoGDIα

ASJC Scopus subject areas

  • Urology
  • Oncology

Cite this

RhoGDIα suppresses growth and survival of prostate cancer cells. / Zhu, Yezi; Tummala, Ramakumar; Liu, Chengfei; Nadiminty, Nagalakshmi; Lou, Wei; Evans, Christopher P; Zhou, Qinghua; Gao, Allen C.

In: Prostate, Vol. 72, No. 4, 03.2012, p. 392-398.

Research output: Contribution to journalArticle

Zhu, Y, Tummala, R, Liu, C, Nadiminty, N, Lou, W, Evans, CP, Zhou, Q & Gao, AC 2012, 'RhoGDIα suppresses growth and survival of prostate cancer cells', Prostate, vol. 72, no. 4, pp. 392-398. https://doi.org/10.1002/pros.21441
Zhu Y, Tummala R, Liu C, Nadiminty N, Lou W, Evans CP et al. RhoGDIα suppresses growth and survival of prostate cancer cells. Prostate. 2012 Mar;72(4):392-398. https://doi.org/10.1002/pros.21441
Zhu, Yezi ; Tummala, Ramakumar ; Liu, Chengfei ; Nadiminty, Nagalakshmi ; Lou, Wei ; Evans, Christopher P ; Zhou, Qinghua ; Gao, Allen C. / RhoGDIα suppresses growth and survival of prostate cancer cells. In: Prostate. 2012 ; Vol. 72, No. 4. pp. 392-398.
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N2 - BACKGROUND Treatment for primary prostate cancer (CaP) is the withdrawal of androgens. However, CaP eventually progresses to grow in a castration-resistant state. The mechanisms involved in the development and progression of castration-resistant prostate cancer (CRPC) remain unknown. We have previously generated LNCaP-IL6+ cells by treating LNCaP cells chronically with interleukin-6 (IL-6), which have acquired the ability to grow in androgen-deprived conditions. METHODS We compared the protein expression profile of LNCaP and LNCaP-IL6+ cells using two-dimensional gel electrophoresis. The gels were then silver stained in order to visualize proteins and the differentially expressed spots were identified and characterized by micro sequencing using MALDI-PMF mass spectrometry. RESULTS In this study, we have identified RhoGDIα (GDIα) as a suppressor of CaP growth. Expression of GDIα was reduced in LNCaP-IL6+ cells and was down-regulated in more aggressive CaP cells compared to LNCaP cells. Over expression of GDIα inhibited the growth of CaP cells and caused LNCaP-IL6+ cells reversal to androgen-sensitive state, while down-regulation of GDIα enhanced growth of androgen-sensitive LNCaP CaP cells in androgen-deprived conditions. In addition, GDIα suppressed the tumorigenic ability of prostate tumor xenografts in vivo. CONCLUSIONS These results demonstrate that loss of GDIα expression promotes the development and progression of prostate cancer.

AB - BACKGROUND Treatment for primary prostate cancer (CaP) is the withdrawal of androgens. However, CaP eventually progresses to grow in a castration-resistant state. The mechanisms involved in the development and progression of castration-resistant prostate cancer (CRPC) remain unknown. We have previously generated LNCaP-IL6+ cells by treating LNCaP cells chronically with interleukin-6 (IL-6), which have acquired the ability to grow in androgen-deprived conditions. METHODS We compared the protein expression profile of LNCaP and LNCaP-IL6+ cells using two-dimensional gel electrophoresis. The gels were then silver stained in order to visualize proteins and the differentially expressed spots were identified and characterized by micro sequencing using MALDI-PMF mass spectrometry. RESULTS In this study, we have identified RhoGDIα (GDIα) as a suppressor of CaP growth. Expression of GDIα was reduced in LNCaP-IL6+ cells and was down-regulated in more aggressive CaP cells compared to LNCaP cells. Over expression of GDIα inhibited the growth of CaP cells and caused LNCaP-IL6+ cells reversal to androgen-sensitive state, while down-regulation of GDIα enhanced growth of androgen-sensitive LNCaP CaP cells in androgen-deprived conditions. In addition, GDIα suppressed the tumorigenic ability of prostate tumor xenografts in vivo. CONCLUSIONS These results demonstrate that loss of GDIα expression promotes the development and progression of prostate cancer.

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