TY - JOUR
T1 - A human novel gene DERPC located on 16q22.1 inhibits prostate tumor cell growth and its expression is decreased in prostate and renal tumors
AU - Sun, Mei
AU - Ma, Lanfeng
AU - Xu, Linda
AU - Li, Jia
AU - Zhang, Wei
AU - Petrovics, Gyorgy
AU - Makarem, Mazen
AU - Sesterhenn, Isabell
AU - Zhang, Mei
AU - Blanchette-Mackie, E. Joan
AU - Moul, Judd
AU - Srivastava, Shiv
AU - Zou, Zhiqiang
PY - 2002/10/1
Y1 - 2002/10/1
N2 - Background: Deletion of chromosome 16q is frequently associated with diverse tumors. Numerous studies strongly suggest the presence of one or more tumor suppressor genes on chromosome 16q22 to 16qter including the widely studied cadherin gene family. However, the specific tumor suppressor genes residing in this region need better definition and characterization. Material and Methods: Standard molecular biology approaches have been used to clone and characterize the DERPC cDNA and its protein product on chromosome 16q22.1. Northern blotting was used to define the expression pattern in a multiple human tissue blots. DERPC expression was examined in multi-tumor array (Clontech, CA, USA) dot blot as well as in laser capture microdissection (LCM) derived prostate cancer (CAP) specimens by quantitative RT-PCR. Western blot analysis and a fluorescent microscopy were used to characterize the molecular size and the cellular location of green fluorescent protein (GFP)-tagged DERPC fusion proteins. A colony formation assay was conducted to determine the effects of DERPC expression on tumor cell growth. Results: A novel gene DERPC (Decreased Expression in Renal and Prostate Cancer) was identified and characterized. DERPC encoded a strong basic, proline- and glycine-rich nuclear protein. DERPC was ubiquitously expressed, with abundant expression in kidney, skeletal muscle, testis, liver, ovary, and heart and moderate expression in prostate. DERPC expression was reduced in renal (67%) and prostate tumors (33%). Expression of DERPC has inhibitory potential on CaP cell growth. Further, overexpression of DERPC in LNCaP cells caused alterations of nuclear morphology. Conclusion: This study suggests that decreased expression of DERPC may be implicated in tumorigenesis of renal and CaPs.
AB - Background: Deletion of chromosome 16q is frequently associated with diverse tumors. Numerous studies strongly suggest the presence of one or more tumor suppressor genes on chromosome 16q22 to 16qter including the widely studied cadherin gene family. However, the specific tumor suppressor genes residing in this region need better definition and characterization. Material and Methods: Standard molecular biology approaches have been used to clone and characterize the DERPC cDNA and its protein product on chromosome 16q22.1. Northern blotting was used to define the expression pattern in a multiple human tissue blots. DERPC expression was examined in multi-tumor array (Clontech, CA, USA) dot blot as well as in laser capture microdissection (LCM) derived prostate cancer (CAP) specimens by quantitative RT-PCR. Western blot analysis and a fluorescent microscopy were used to characterize the molecular size and the cellular location of green fluorescent protein (GFP)-tagged DERPC fusion proteins. A colony formation assay was conducted to determine the effects of DERPC expression on tumor cell growth. Results: A novel gene DERPC (Decreased Expression in Renal and Prostate Cancer) was identified and characterized. DERPC encoded a strong basic, proline- and glycine-rich nuclear protein. DERPC was ubiquitously expressed, with abundant expression in kidney, skeletal muscle, testis, liver, ovary, and heart and moderate expression in prostate. DERPC expression was reduced in renal (67%) and prostate tumors (33%). Expression of DERPC has inhibitory potential on CaP cell growth. Further, overexpression of DERPC in LNCaP cells caused alterations of nuclear morphology. Conclusion: This study suggests that decreased expression of DERPC may be implicated in tumorigenesis of renal and CaPs.
UR - http://www.scopus.com/inward/record.url?scp=20244385234&partnerID=8YFLogxK
U2 - 10.1007/bf03402176
DO - 10.1007/bf03402176
M3 - Article
C2 - 12477976
AN - SCOPUS:20244385234
SN - 1076-1551
VL - 8
SP - 655
EP - 663
JO - Molecular medicine (Cambridge, Mass.)
JF - Molecular medicine (Cambridge, Mass.)
IS - 10
ER -