title: The altered expression of MiR-221/-222 and MiR-23b/-27b is associated with the development of human castration resistant prostate cancer.
abstract: BACKGROUND
  We have previously identified seven miRs-miR-221, -222, -23b, -27b, -15a, -16-1, and -203, that are differentially expressed in the hormone sensitive LNCaP cell line and the hormone resistant LNCaP-abl cell line and hypothesized that these miRs may characterize certain subtypes of human castration resistant prostate cancer (CRPC).
  
  
  METHODS
  Functional studies in cell culture systems have been performed to determine the effect of alternated expression level on cellular response to androgen treatment. To determine the clinical relevance of the expression patterns of these miRs, we compared the expression levels of these seven miRs in normal prostate tissues from 86 individuals, prostate tumor tissues from 34 individuals with localized hormone naïve disease, and bone-derived metastatic CRPC tissues from 17 individuals.
  
  
  RESULTS
  The altered expression of miR-221/-222 (as previously described) or miR-203 affected the cellular response to androgen treatment, suggesting their potential involvement in the transition to CRPC. However, the expression of miR-23b, -27b, -15a, and -16-1 did not have a significant influence in the cellular response to androgen treatment, suggesting that these miRs may not play a causative role in the CRPC phenotype. Comparison of the expression levels of these miRs in tissue samples revealed that strikingly, ∼90% of the analyzed metastatic CRPC tumors could be characterized by the increased miR-221/-222 expression and the down-regulated miR-23b/-27b expression.
  
  
  CONCLUSIONS
  This finding suggests that altered miR-221/-222 and miR-23b/-27b expression may be associated with the CRPC process.
authors: Departmentof Medical Oncology, Dana Farber Cancer, Institute, Harvard Medical School, 450 Brookline Ave., Boston, Massachusetts 02115.
authors: Tong
authors: T
authors: Sun
authors: Departmentof Medical Oncology, Dana Farber Cancer, Institute, Harvard Medical School, 450 Brookline Ave., Boston, Massachusetts 02115.
authors: Ming
authors: M
authors: Yang
authors: Departmentof Medicine, Beth Israel Deaconess Medical, Center, Harvard Medical School, 330 Brookline Ave., Boston, Massachusetts 02115.
authors: Shaoyong
authors: S
authors: Chen
authors: Departmentof Medicine, Beth Israel Deaconess Medical, Center, Harvard Medical School, 330 Brookline Ave., Boston, Massachusetts 02115.
authors: Steven
authors: S
authors: Balk
authors: Departmentof Medical Oncology, Dana Farber Cancer, Institute, Harvard Medical School, 450 Brookline Ave., Boston, Massachusetts 02115.
authors: Mark
authors: M
authors: Pomerantz
authors: Departmentof Medical Oncology, Dana Farber Cancer, Institute, Harvard Medical School, 450 Brookline Ave., Boston, Massachusetts 02115.
authors: Chen-Lin
authors: CL
authors: Hsieh
authors: Departmentof Medical Oncology, Dana Farber Cancer, Institute, Harvard Medical School, 450 Brookline Ave., Boston, Massachusetts 02115.
authors: Myles
authors: M
authors: Brown
authors: Departmentof Medical Oncology, Dana Farber Cancer, Institute, Harvard Medical School, 450 Brookline Ave., Boston, Massachusetts 02115.
authors: Gwo-Shu Mary
authors: GM
authors: Lee
authors: Departmentof Medical Oncology, Dana Farber Cancer, Institute, Harvard Medical School, 450 Brookline Ave., Boston, Massachusetts 02115.
authors: Philip W
authors: PW
authors: Kantoff
mesh_terms: D045744:Cell Line, Tumor; D018450:Disease Progression; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D009919:Orchiectomy; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology
chemical_list: D035683:MicroRNAs; C525709:MIR221, human; C525710:MIR222, human; C552430:MIRN23a microRNA, human; C531388:MIRN27 microRNA, human