Corina Junquera

Publications (2)10.73 Total impact

• Article: Plexin B1 is downregulated in renal cell carcinomas and modulates cell growth.

  J Javier Gómez Román, Gorka Ochoa Garay, Pilar Saenz, Kepa Escuredo, Cristina Sanz Ibayondo, Silvio Gutkind, Corina Junquera, Laureano Simón, Antonio Martínez, José Luis Fernández Luna, J Fernando Val-Bernal
  [show abstract] [hide abstract]
  ABSTRACT: Plexins are a family of transmembrane receptors that interact with the repulsive axon guidance molecules (Semaphorins) in neural tissues. In extraneural tissues, plexins are involved in other cellular functions often altered in neoplastic cells, such as adhesion, migration, and apoptosis. Plexin B1 has been implicated in the regulation of Akt, which is an activated pathway in renal cell neoplasms, and only 1 report has emphasized its role as an oncogenic factor. Furthermore, plexin B1 is located in 3p21, which is a chromosomal region deleted frequently in renal cell carcinomas. In accordance with a hypothetical oncogenic role for plexin B1, we have shown by reverse transcription-polymerase chain reaction that plexin B1 is expressed in nonneoplastic renal tissue, and it is severely downregulated in clear cell renal carcinomas. We have also demonstrated by immunohistochemistry on tissue microarrays that plexin B1 protein is absent in more than 80% of renal cell carcinomas (169 in 209 carcinomas examined). Otherwise, all kinds of renal tubules showed strong membrane reactivity. Moreover, when we have induced plexin B1 expression with an expression vector in the renal adenocarcinoma cell line ACHN, a marked reduction in proliferation rate was produced. Altogether, this evidence suggests a possible role for plexin B1 in renal oncogenesis.
  Translational Research 04/2008; 151(3):134-40. · 2.99 Impact Factor
• Source

  Available from: Simon Santa Cruz

  Article: Fibroblast growth factor receptor 3 is overexpressed in urinary tract carcinomas and modulates the neoplastic cell growth.

  J Javier Gómez-Román, Pilar Saenz, Miguel Molina, Jorge Cuevas González, Kepa Escuredo, Simon Santa Cruz, Corina Junquera, Laureano Simón, Antonio Martínez, J Luis Gutiérrez Baños, Marta López-Brea, Clara Esparza, J Fernando Val-Bernal
  [show abstract] [hide abstract]
  ABSTRACT: Fibroblast growth factor receptor 3 (FGFR3) mutations have been associated with achondroplastic syndromes and urinary bladder carcinomas. Here we describe changes in FGFR3 mRNA and protein expression in transitional carcinomas and determine the effect of monoclonal antibodies against FGFR3 in RT-112 cell line proliferation. We used microarray tools to evaluate FGFR3 mRNA expression in 22 urinary bladder carcinomas at different stages (noninvasive pTa, lamina propria invasive pT1, and muscular invasive pT2) and 7 nonneoplastic tissue controls. FGFR3 protein expression was evaluated by Western blotting in 15 different carcinomas and 3 nonneoplastic controls. Two hundred thirty-seven urinary bladder and renal pelvis carcinomas and 21 negative controls were tested on tissue microarrays by immunohistochemistry. The effect on cell proliferation in the RT-112 bladder cancer cell line of monoclonal antibodies against FGFR3 was also evaluated. Overexpression of FGFR3 mRNA was found in pTa and pT1 stage carcinomas (fold change >8) and in pT2 carcinomas (fold change >4). Nonneoplastic urinary bladder samples do not express FGFR3 protein. However, 83% of pTa, 100% of pT1, and 50% of pT2 carcinomas expressed FGFR3 as determined by Western blotting. By immunohistochemistry, FGFR3 was positive in 71.4% of pTa, 72% of pT1, and 49.2% of pT2 cases as well as 61.5% of upper urinary tract carcinomas. Proliferation of the RT-112 cell line was inhibited with monoclonal antibodies against FGFR3. FGFR3 seems to play an important role in transitional cell carcinoma development. Our results suggest that FGFR3 antagonists could be developed as possible therapeutics for treatment of urinary tract carcinoma.
  Clinical Cancer Research 02/2005; 11(2 Pt 1):459-65. · 7.74 Impact Factor