c-Jun activation in acquired cystic kidney disease and renal cell carcinoma

Mototsugu Oya, Shuji Mikami, Ryuichi Mizuno, Ken Marumo, Makio Mukai, Masaru Murai

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Purpose: Activator protein-1 has a central role in transducing cytokine signals. Activator protein-1 is composed of 2 proto-oncogene families, namely Jun and Fos. Of them c-Jun has been suggested to have a role in cell cycle progression and neoplastic transformation. We examined the impact of c-Jun protein activation on pathological parameters in renal cell carcinoma (RCC). Materials and Methods: The expression of total c-Jun protein and phosphorylated c-Jun protein was determined by immunohistochemistry in 72 patients with RCC, including 10 with tumor arising from acquired cystic kidney disease (ACKD) of end stage kidneys. Results: c-Jun expression was observed in the distal but not the proximal tubules. Atypical hyperplastic cells in ACKD were positive for phosphorylated c-Jun. RCC arising in end stage kidneys was pT1 and 5 of these cases showed increased c-Jun activation. Of 62 cases arising from normally functioning kidneys 21 showed an increased degree of c-Jun activation. In localized small cell cases (pT1a) 55.5% (10 of 18) showed enhanced activation, whereas such enhanced activation was only observed in 25% (11 of 44) of more advanced cases (pT1b or greater). Therefore, c-Jun activation was considered to be related to the early carcinogenesis of RCC. Conclusions: This study emphasizes the role that c-Jun activation has in early RCC carcinogenesis. Thus, chronic stimulation of cytokines inducing c-Jun activation may have a role in the aberrant proliferation of hyperplastic atypical cells in ACKD and RCC.

Original languageEnglish
Pages (from-to)726-730
Number of pages5
JournalJournal of Urology
Volume174
Issue number2
DOIs
Publication statusPublished - 2005 Aug

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Cystic Kidney Diseases
Renal Cell Carcinoma
Proto-Oncogene Proteins c-jun
Transcription Factor AP-1
Kidney
Carcinogenesis
Cytokines
Proto-Oncogenes
Cell Cycle
Immunohistochemistry
Neoplasms

Keywords

  • Carcinoma, renal cell
  • Genes, jun
  • Kidney
  • Polycystic kidney diseases
  • Renal dialysis

ASJC Scopus subject areas

  • Urology

Cite this

c-Jun activation in acquired cystic kidney disease and renal cell carcinoma. / Oya, Mototsugu; Mikami, Shuji; Mizuno, Ryuichi; Marumo, Ken; Mukai, Makio; Murai, Masaru.

In: Journal of Urology, Vol. 174, No. 2, 08.2005, p. 726-730.

Research output: Contribution to journalArticle

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abstract = "Purpose: Activator protein-1 has a central role in transducing cytokine signals. Activator protein-1 is composed of 2 proto-oncogene families, namely Jun and Fos. Of them c-Jun has been suggested to have a role in cell cycle progression and neoplastic transformation. We examined the impact of c-Jun protein activation on pathological parameters in renal cell carcinoma (RCC). Materials and Methods: The expression of total c-Jun protein and phosphorylated c-Jun protein was determined by immunohistochemistry in 72 patients with RCC, including 10 with tumor arising from acquired cystic kidney disease (ACKD) of end stage kidneys. Results: c-Jun expression was observed in the distal but not the proximal tubules. Atypical hyperplastic cells in ACKD were positive for phosphorylated c-Jun. RCC arising in end stage kidneys was pT1 and 5 of these cases showed increased c-Jun activation. Of 62 cases arising from normally functioning kidneys 21 showed an increased degree of c-Jun activation. In localized small cell cases (pT1a) 55.5{\%} (10 of 18) showed enhanced activation, whereas such enhanced activation was only observed in 25{\%} (11 of 44) of more advanced cases (pT1b or greater). Therefore, c-Jun activation was considered to be related to the early carcinogenesis of RCC. Conclusions: This study emphasizes the role that c-Jun activation has in early RCC carcinogenesis. Thus, chronic stimulation of cytokines inducing c-Jun activation may have a role in the aberrant proliferation of hyperplastic atypical cells in ACKD and RCC.",
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AU - Mukai, Makio

AU - Murai, Masaru

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