RFC2 promotes aerobic glycolysis and progression of colorectal cancer.
Aerobic glycolysis
CREB5
Colorectal cancer
MET/PI3K/AKT/mTOR
RFC2
Journal
BMC gastroenterology
ISSN: 1471-230X
Titre abrégé: BMC Gastroenterol
Pays: England
ID NLM: 100968547
Informations de publication
Date de publication:
11 Oct 2023
11 Oct 2023
Historique:
received:
18
04
2023
accepted:
29
09
2023
medline:
13
10
2023
pubmed:
12
10
2023
entrez:
11
10
2023
Statut:
epublish
Résumé
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). 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. RFC2 promoted the progression of CRC cells via activating aerobic glycolysis and the MET/PI3K/AKT/mTOR pathway.
Sections du résumé
BACKGROUND
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
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
CONCLUSIONS
RFC2 promoted the progression of CRC cells via activating aerobic glycolysis and the MET/PI3K/AKT/mTOR pathway.
Identifiants
pubmed: 37821801
doi: 10.1186/s12876-023-02984-0
pii: 10.1186/s12876-023-02984-0
pmc: PMC10566032
doi:
Substances chimiques
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Phosphatidylinositol 3-Kinases
EC 2.7.1.-
Replication Protein C
EC 3.6.4.-
TOR Serine-Threonine Kinases
EC 2.7.11.1
RFC2 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
353Informations de copyright
© 2023. BioMed Central Ltd., part of Springer Nature.
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