Lack of relation of AKAP12 with p53 and Bcl-2 in colorectal carcinoma

Asian Pac J Cancer Prev. 2014;15(8):3415-8. doi: 10.7314/apjcp.2014.15.8.3415.

Abstract

Background: AKAP12 inhibits oncogenic proliferation, invasion, chemotaxis and neovascularization. Bcl-2 and p53 are two important apoptotic markers that play roles in apoptotic processes. It has been found that AKAP12 blocks the cell cycle and induces apoptosis in fibrosarcoma cells. In our study we assessed the relationship of AKAP12 with apoptotic markers, Bcl-2 and p53.

Materials and methods: Our study included 45 cases that were histopathologically diagnosed with colorectal carcinoma from the tissue samples acquired by surgical resection. AKAP 12, Bcl-2, and p53 expression was examined by immunohistochemistry.

Results: A total of 45 colorectal adenocarcinoma patients - 17 (37.8%) females and 28 (62.2%) males - were included in this study. AKAP12 expression was found to be negative in 8 patients (17.8%), and positive in 37 patients (82.2%). Bcl-2 was found positive in 6 patients (13.3%) and p53 in 29 patients (55.6%). AKAP12 expression had no significant relation with Bcl-2 and p53 expression (p:0.939, p:0.079, respectively).

Conclusions: Although various studies have pointed to apoptotic activity of AKAP12, the literature is limited regarding relations with p53 or Bcl-2 expression. In the present study, we found no relation in colorectal carcinomas.

MeSH terms

  • A Kinase Anchor Proteins / metabolism*
  • Adenocarcinoma / metabolism*
  • Aged
  • Apoptosis / physiology
  • Biomarkers, Tumor / metabolism*
  • Cell Cycle Proteins / metabolism*
  • Colorectal Neoplasms / metabolism*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • A Kinase Anchor Proteins
  • AKAP12 protein, human
  • Biomarkers, Tumor
  • Cell Cycle Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53