Ribosomal protein S27-like in colorectal cancer: a candidate for predicting prognoses

PLoS One. 2013 Jun 24;8(6):e67043. doi: 10.1371/journal.pone.0067043. Print 2013.

Abstract

Background: The development and progression of colorectal cancer (CRC) involve a complex process of multiple genetic changes. Tumor suppressor p53 is capable of determining the fate of CRC cells. However, the role of a p53-inducible modulator, ribosomal protein S27-like (RPS27L), in CRC is unknown.

Methods: Here, the differential expression of RPS27L was examined in the feces and colonic tissues of CRC patients, to explore its possible correlation with patient survival and to investigate the cellular mechanisms underlying their clinical outcomes. Eighty intermediate-stage CRC patients (42 at stage II and 38 at stage III) were divided into two groups according to their fecal RPS27L mRNA levels. The survival probabilities of the groups were estimated using the Kaplan-Meier method. The RPS27L protein in the colonic tissues of stage III patients with different prognoses was further examined immunohistochemically. RPS27L expression in LoVo cells was manipulated to examine the possible cellular responses in vitro.

Results: Elevated RPS27L expression, in either feces or tissues, was related to a better prognosis. In vitro, RPS27L-expressing LoVo cells ceased DNA synthesis and apoptotic activity while the expression of their DNA repair molecules was upregulated.

Conclusions: Elevated RPS27L may improve the prognoses of certain CRC patients by enhancing the DNA repair capacity of their colonic cells, and can be determined in feces. By integrating clinical, molecular, and cellular data, our study demonstrates that fecal RPS27L may be a useful index for predicting prognoses and guiding personalized therapeutic strategies, especially in patients with intermediate-stage CRC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Cell Line, Tumor
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms / metabolism*
  • Colorectal Neoplasms / pathology
  • DNA Breaks, Double-Stranded
  • DNA Repair
  • Down-Regulation / genetics
  • Feces
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Metalloproteins / genetics
  • Metalloproteins / metabolism*
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Prognosis
  • Proportional Hazards Models
  • Protein Transport
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / metabolism*
  • Ribosomal Proteins / genetics
  • Ribosomal Proteins / metabolism*
  • Survival Analysis

Substances

  • Metalloproteins
  • Nuclear Proteins
  • RNA-Binding Proteins
  • RPS27 protein, human
  • RPS27L protein, human
  • Ribosomal Proteins

Grants and funding

This work was supported by NSC96–2320-B-281–001-MY3 and NSC100-2320-B-281-001 from the National Science Council, and CGH-MR-9919 from Cathay General Hospital. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.