Small ribosomal protein subunit S7 suppresses ovarian tumorigenesis through regulation of the PI3K/AKT and MAPK pathways

PLoS One. 2013 Nov 11;8(11):e79117. doi: 10.1371/journal.pone.0079117. eCollection 2013.

Abstract

Small ribosomal protein subunit S7 (RPS7) has been reported to be associated with various malignancies, but the role of RPS7 in ovarian cancer remains unclear. In this study, we found that silencing of RPS7 by a specific shRNA promoted ovarian cancer cell proliferation, accelerated cell cycle progression, and slightly reduced cell apoptosis and response to cisplatin treatment. Knockdown of RPS7 resulted in increased expression of P85α, P110α, and AKT2. Although the basal levels of ERK1/2, MEK1/2, and P38 were inconsistently altered in ovarian cancer cells, the phosphorylated forms of MEK1/2 (Ser217/221), ERK1/2 (Thr202/Tyr204), JNK1/2 (Thr183/Tyr185), and P38 (Thr180/Tyr182) were consistently reduced after RPS7 was silenced. Both the in vitro anchorage-independent colony formation and in vivo animal tumor formation capability of cells were enhanced after RPS7 was depleted. We also showed that silencing of RPS7 enhanced ovarian cancer cell migration and invasion. In sum, our results suggest that RPS7 suppresses ovarian tumorigenesis and metastasis through PI3K/AKT and MAPK signal pathways. Thus, RPS7 may be used as a potential marker for diagnosis and treatment of ovarian cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Class Ia Phosphatidylinositol 3-Kinase / biosynthesis*
  • Class Ia Phosphatidylinositol 3-Kinase / genetics
  • Extracellular Signal-Regulated MAP Kinases / genetics
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Female
  • Gene Expression Regulation, Enzymologic / genetics
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • MAP Kinase Signaling System*
  • Male
  • Mice
  • Mice, Nude
  • Ovarian Neoplasms / genetics
  • Ovarian Neoplasms / metabolism*
  • Ovarian Neoplasms / pathology
  • Proto-Oncogene Proteins c-akt / biosynthesis*
  • Proto-Oncogene Proteins c-akt / genetics
  • Ribosomal Proteins / genetics
  • Ribosomal Proteins / metabolism*

Substances

  • Ribosomal Proteins
  • ribosomal protein S7
  • Class Ia Phosphatidylinositol 3-Kinase
  • AKT2 protein, human
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases

Grants and funding

This work was supported by National Nature Science Foundation of China (#91129721) for Gong Yang and Young Backbone Foundation of Fudan University (11L-38B) for Ziliang Wang. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.