LncRNA EGOT Promotes Tumorigenesis Via Hedgehog Pathway in Gastric Cancer

Pathol Oncol Res. 2019 Jul;25(3):883-887. doi: 10.1007/s12253-017-0367-3. Epub 2017 Dec 5.

Abstract

Gastric cancer (GC) is one of the mostly terminal malignancies with poor prognosis. Long noncoding RNA EGOT (EGOT) acts as a crucial regulator in the breast cancer. However, the function of EGOT in GC remains unknown. This work was to explore the clinical value and biological significance of EGOT in GC. EGOT levels in GC tissue and cell were analyzed by qRT-PCR. After knockdown of EGOT, GC cell growth and cycle progression were detected. The expression of EGOT was observably elevated in GC. Upregulation of EGOT was related with lymphatic metastasis and TNM stage. In addition, knockdown of EGOT by siRNA could significantly inhibit GC cell proliferation and arrest cycle progression in G1 phase. Moreover, EGOT mediated cyclin D1 expression in GC cells which was regulated by Hedgehog pathway. Further, loss of EGOT downregulated Hedgehog signaling pathway in GC cells. EGOT functions as an oncogene in GC, and may be useful as a conceivable diagnostic and prognostic biomarker for GC tumorigenesis.

Keywords: EGOT; Gastric cancer; Hedgehog; Tumorigenesis; lncRNA.

MeSH terms

  • Apoptosis / genetics
  • Biomarkers, Tumor / genetics
  • Carcinogenesis / genetics*
  • Carcinogenesis / pathology
  • Cell Line
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Cyclin D1 / genetics
  • Disease Progression
  • Down-Regulation / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / genetics
  • Hedgehog Proteins / genetics*
  • Humans
  • Lymphatic Metastasis / genetics
  • Lymphatic Metastasis / pathology
  • Male
  • Middle Aged
  • RNA, Long Noncoding / genetics*
  • Signal Transduction / genetics*
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / pathology
  • Up-Regulation / genetics

Substances

  • Biomarkers, Tumor
  • EGOT lncRNA, human
  • Hedgehog Proteins
  • RNA, Long Noncoding
  • Cyclin D1