title: Remnant lipoproteins induced proliferation of human prostate cancer cell, PC-3 but not LNCaP, via low density lipoprotein receptor.
abstract: BACKGROUND
  Hypertriglyceridemia has been shown to be one of the risk factors for prostate cancer. In this study, we investigated the effect of remnant lipoproteins on cell growth in prostate cancer cell lines.
  
  
  METHODS
  Remnant lipoproteins were isolated as remnant like particles (RLP) from human plasma. We used RLP for TG-rich lipoproteins and low density lipoproteins (LDL) for cholesterol-rich lipoproteins respectively and examined the effect of lipoproteins on proliferation of PC-3 and LNCaP cells using MTS assays. Moreover, we studied the effect of RLP and LDL treatment on the regulation of lipoprotein receptors in prostate cancer cells to investigate the relationship between lipoprotein-induced cell proliferation and lipoprotein receptor expression using real-time PCR, Western blotting assays and siRNA.
  
  
  RESULTS
  RLP effectively induced PC-3 cell proliferation more than LDL, whereas both RLP and LDL could not induce LNCaP cell proliferation except at a higher concentration of RLP. LDL receptor (LDLr) was expressed in both prostate cancer cells but there was a sharp difference of sterol regulation between two cells. In PC-3 cells, LDL decreased the LDLr expression in some degree, but RLP did not. Meanwhile LDLr expression in LNCaP was easily downregulated by RLP and LDL. Blocking LDLr function significantly inhibited both RLP- and LDL-induced PC-3 cell proliferation.
  
  
  CONCLUSIONS
  This study demonstrated that RLP-induced PC-3 cell proliferation more than LDL; however, both RLP and LDL hardly induced LNCaP cell proliferation. The differences of proliferation by lipoproteins might be involved in the regulation of LDLr expression.
authors.affiliation: Department of Urology, Gunma University Graduate School of Medicine, Maebashi, Gunma-pref, Japan.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Sekine
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Koike
authors.forename: Takamitsu
authors.initials: T
authors.lastname: Nakano
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Nakajima
authors.forename: Sadao
authors.initials: S
authors.lastname: Takahashi
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Suzuki
mesh_terms: D000704:Analysis of Variance; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D002784:Cholesterol; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D015228:Hypertriglyceridemia / Q000150:complications / Q000378:metabolism; D008074:Lipoproteins / Q000378:metabolism*; D008297:Male; D011471:Prostatic Neoplasms / Q000378:metabolism* / Q000473:pathology*; D012313:RNA / Q000032:analysis; D011973:Receptors, LDL / Q000378:metabolism*; D051782:Sterol Regulatory Element Binding Protein 2 / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D008074:Lipoproteins; D011973:Receptors, LDL; C497390:SREBF2 protein, human; D051782:Sterol Regulatory Element Binding Protein 2; D014280:Triglycerides; C112017:remnant-like particle cholesterol; D012313:RNA; D002784:Cholesterol