TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000321358
  • Gene Name:YBX1
  • mRNA database:Ensembl
  • mRNA expression :up-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:NA
  • Evidence:predicted
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:NA
  • Drug Method:NA

Disease basic infommation

  • Disease:colon cancer
  • Tissue:Five human colon cancer cell lines, T84, HT29, HCT116, CaCo2 and SW480

Other information

  • Title:Y-box-binding protein?1 inhibits apoptosis and upregulates EGFR in colon cancer.
  • Journal:Oncol Rep
  • Published:2019
  • PubMed ID:30864697
  • Abstract:Y-box-binding protein 1 (YB-1) is a DNA/RNA--binding protein and an important transcription and translation factor in carcinogenesis. However, the biological function and molecular correlation of YB-1 in colorectal cancer are not fully understood. The aim of the present study was to determine the significance of YB-1 expression and its biological role in colorectal cancer. Cell proliferation, migration and apoptosis were examined upon knockdown of YB-1 expression in different colon cancer cell lines that had different genetic backgrounds. Since the properties of different colon cancer cell lines with specific RAS/RAF gene mutations downstream epidermal growth factor receptor (EGFR) may differ from wild-type colorectal cancer, it is critical to study the role of YB-1 with respect to the mutational status of RAS. The results indicated that the suppression of YB-1 decreased cell proliferation (P<0.05) and migration (P<0.05) regardless of the status of RAS/RAF in the HT29, HCT116 and CaCo2 cell lines. In contrast, YB-1 knockdown altered the expression of apoptosis-related genes and the expression of EGFR was detected in the cell lines expressing wild-type RAS/RAF but not in those expressing mutated RAS/RAF. These results indicated that YB-1 plays an important role in cell proliferation, migration, apoptosis and EGFR expression in colorectal cancer. Furthermore, apoptosis and EGFR expression may be affected by the mutational status of RAS/RAF and controlled through YB-1.
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