Korean J Urol.  2006 Jun;47(6):661-666. 10.4111/kju.2006.47.6.661.

Downregulation of Peroxisome Proliferator-Activated Receptor (PPAR)alpha, PPARgamma, and Phosphoglycerate Mutase 2 in Prostate Cancer

Affiliations
  • 1Department of Urology, Catholic University of Daegu School of Medicine, Daegu, Korea. dykim@mail.cu.ac.kr
  • 2Department of Physiology, Kyungpook National University School of Medicine, Daegu, Korea.
  • 3Department of Urology, Eulji University School of Medicine, Seoul, Korea.

Abstract

PURPOSE: To evaluate whether factors related to lipid and glucose metabolism have a potential role in the progression of prostate cancer, we measured the mRNA levels of the peroxisome proliferator-activated receptor (PPAR), fatty acid elongase (ELOVL), and two glycolytic enzymes in prostate cancer (CaP) tissues.
MATERIALS AND METHODS
Prostate tissues, obtained from radical prostatectomy (n=10) and transurethral resection of prostate (n=18), were quickly frozen in liquid nitrogen for RNA measurements. Transcript signals of PPAR alpha, PPAR gamma, ELOVL2, ELOVL5, phosphoglycerate kinase 1 (PgK1) and phosphoglycerate mutase 2 (PgM2) were measured using a reverse-transcription polymerase chain reaction.
RESULTS
The transcript signals of PPAR alpha and PPAR gamma were down-regulated in CaP tissues. In addition, the mRNA level of PgM2 in CaP tissues was lower than that in benign prostatic hyperplasia (BPH) tissues. However, the messages for ELOVL2, ELOVL5, and PgK1 were not significantly changed.
CONCLUSIONS
These results suggest that lowering of the PPARalpha, PPARgamma and PgM2 messages may be involved in aberrant and uncontrolled prostate cell growth and differentiation.

Keyword

Prostate cancer; Peroxisome proliferator-activated receptors; Phosphoglycerate mutase

MeSH Terms

Down-Regulation*
Glucose
Metabolism
Nitrogen
Peroxisome Proliferator-Activated Receptors
Peroxisomes*
Phosphoglycerate Kinase
Phosphoglycerate Mutase*
Polymerase Chain Reaction
PPAR alpha
PPAR gamma*
Prostate*
Prostatectomy
Prostatic Hyperplasia
Prostatic Neoplasms*
RNA
RNA, Messenger
Transurethral Resection of Prostate
Glucose
Nitrogen
PPAR alpha
PPAR gamma
Peroxisome Proliferator-Activated Receptors
Phosphoglycerate Kinase
Phosphoglycerate Mutase
RNA
RNA, Messenger

Figure

  • Fig. 1 Representative examples (upper panel) and densitometric analyses (lower panel) of the polymerase chain reaction (PCR) products for peroxisome proliferator-activated receptor (PPAR)α and PPARγ, corrected for the 18S rRNA value, in each sample. The values are expressed in arbitrary densitometric units (A.D.U.) as the mean±SE of human prostate tissue; either benign prostatic hyperplasia (BPH) or prostate cancer (CaP). *p<0.05, vs. BPH (Mann-Whitney test).

  • Fig. 2 Representative examples (upper panel) and densitometric analyses (lower panel) of the polymerase chain reaction (PCR) products for fatty acid elongase (ELOVL) 2 and ELOVL5, corrected for 18S rRNA or β-actin, respectively, in each sample. The values are expressed in arbitrary densitometric units (A.D.U.) as the mean±SE of human prostate tissue; either benign prostatic hyperplasia (BPH) or prostate cancer (CaP).

  • Fig. 3 Representative examples (upper panel) and densitometric analyses (lower panel) of the polymerase chain reaction (PCR) products of phosphoglycerate kinase 1 (PgK1) and phosphoglycerate mutase 2 (PgM2), corrected for the 18S rRNA value, in each sample. The values are expressed in arbitrary densitometric units (A.D.U.) as the mean±SE of human prostate tissue; either benign prostatic hyperplasia (BPH) or prostate cancer (CaP). *p< 0.01, vs. BPH (Mann-Whitney test).

  • Fig. 4 Expressions of peroxisome proliferator-activated receptor (PPAR)α, PPARγ and phosphoglycerate kinase 1 (PgK1), corrected for β-actin, in each sample. Values are shown in arbitrary densitometric units (A.D.U.) as the mean±SE of human prostate tissue; either benign prostatic hyperplasia (BPH) or prostate cancer (CaP). *p<0.05, vs. BPH (Mann-Whitney test).


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