ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway

Biomed Res Int. 2021 Jan 22:2021:8971728. doi: 10.1155/2021/8971728. eCollection 2021.

Abstract

Osteosarcoma (OS) is a familiar malignant bone tumor that occurs mainly in adolescents. Immature colon carcinoma transcript-1 (ICT1) is an important member of the large mitoribosomal subunit in mitochondrial ribosomes, which has been shown to be closely related to tumorigenesis. Its expression and function in OS, however, remained unclear. Here, we showed that ICT1 was significantly upregulated in OS and promoted the growth of OS cells. Mechanistically, ICT1 acted as an oncogene in OS and promoted proliferation and inhibited apoptosis of OS cells through the STAT3/BCL-2 axis. These results reveal a novel insight into the role of the ICT1/STAT3/BCL-2 axis in OS and therefore may represent a novel molecular target for novel treatments.

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Cell Line, Tumor
  • Cell Proliferation / genetics*
  • Gene Knockdown Techniques
  • Heterografts
  • Humans
  • Mice
  • Mice, Nude
  • Osteosarcoma* / genetics
  • Osteosarcoma* / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Ribosomal Proteins* / genetics
  • Ribosomal Proteins* / metabolism
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction / genetics
  • Up-Regulation

Substances

  • MRPL58 protein, human
  • Proto-Oncogene Proteins c-bcl-2
  • Ribosomal Proteins
  • STAT3 Transcription Factor
  • STAT3 protein, human