RFC2 promotes aerobic glycolysis and progression of colorectal cancer

BMC Gastroenterol. 2023 Oct 11;23(1):353. doi: 10.1186/s12876-023-02984-0.

Abstract

Background: Replication factor C subunit 2 (RFC2) participates in the growth and metastasis of various malignancies. Our study investigated the roles of RFC2 in colorectal cancer (CRC).

Results: RFC2 expression was upregulated in CRC tissues and cells. High RFC2 expression was associated with poor prognosis. Knockdown RFC2 inhibited proliferation, induced apoptosis, and suppressed migration and invasion of CRC cells. CREB5 was a transcription factor of RFC2, and CREB5 knockdown suppressed RFC2 expression. Furthermore, RFC2 promoted aerobic glycolysis and MET/PI3K/AKT/mTOR pathway.

Conclusion: RFC2 promoted the progression of CRC cells via activating aerobic glycolysis and the MET/PI3K/AKT/mTOR pathway.

Keywords: Aerobic glycolysis; CREB5; Colorectal cancer; MET/PI3K/AKT/mTOR; RFC2.

MeSH terms

  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Colorectal Neoplasms* / pathology
  • Glycolysis
  • Humans
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Replication Protein C / metabolism
  • Signal Transduction*
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Proto-Oncogene Proteins c-akt
  • Phosphatidylinositol 3-Kinases
  • Replication Protein C
  • TOR Serine-Threonine Kinases
  • RFC2 protein, human