PlGF knockdown induced apoptosis through Wnt signaling pathway in gastric cancer stem cells

J Cell Biochem. 2019 Mar;120(3):3268-3276. doi: 10.1002/jcb.27593. Epub 2018 Sep 11.

Abstract

Despite the fact that much research has focused on gastric cancer, it is still a worldwide concern, because of the difficulties with factors such as signaling pathway crosstalk and gastric cancer stem cell (GCSC). Placental growth factor (PlGF) is one of these factors, and its tumorigenicity potential still remains a question. As a result, we have investigated the effect of PlGF knockdown on apoptosis and genes involved in the Wnt signaling pathway, and apoptosis in cancer stem cells derived from AGS an MKN-45 gastric cancer cell lines. We isolated GCSCs from MKN-45 and AGS cell lines on a nonadherent surface. Then the cell viability, the real-time reverse transcription-polymerase chain reaction data of the genes involved in the Wnt signaling pathway, and apoptosis were evaluated. Furthermore, DNA laddering was used to show the apoptotic effect and DNA fragmentation caused by the PlGF knockdown. Our investigation revealed that the PlGF knockdown with PlGF-specific small interfering RNA at 40 pmol for GCSCs derived from MKN-45 and AGS at 24 hours can significantly affect the cell viability, the Wnt signaling pathway, and the apoptosis-related genes expression. In conclusion, we showed the PlGF knockdown may induce apoptosis via the Wnt signaling pathway in GCSCs.

Keywords: Wnt signaling pathway; apoptosis; cancer stem cell (CSC); gastric cancer; gene expression; placental growth factor (PlGF).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Survival / genetics
  • Cell Survival / physiology
  • Humans
  • Neoplastic Stem Cells / cytology*
  • Neoplastic Stem Cells / metabolism*
  • Placenta Growth Factor / genetics
  • Placenta Growth Factor / metabolism*
  • RNA, Small Interfering / genetics
  • Stomach Neoplasms / metabolism*
  • Wnt Signaling Pathway / genetics
  • Wnt Signaling Pathway / physiology

Substances

  • PGF protein, human
  • RNA, Small Interfering
  • Placenta Growth Factor