Activation of DDX58/RIGI suppresses the growth of tumor cells by inhibiting STAT3/CSE signaling in colon cancer.
Int J Oncol
; 61(4)2022 Oct.
Article
en En
| MEDLINE
| ID: mdl-36004488
ABSTRACT
Some patients with colon cancer eventually develop metastasis during treatment, and the 5year survival rate of patients with metastatic colon cancer remains relatively low, which is most likely due to the ineffectiveness of the current standard treatment. Systemic treatment for patients with colon cancer has expanded from chemotherapy to targeted therapy and immunotherapy. Immunotherapy holds promise in the treatment of colon cancer. The present study revealed the role of innate immune receptor helicase DExD/Hbox helicase 58 (DDX58), which encodes retinoic acidinducible geneI (RIGI), in colon cancer. It was demonstrated that colon cancer patients with a low protein expression of DDX58/RIGI had a worse 5year survival rate of patients compared with patients with a high expression of DDX58/RIGI. The activation of DDX58/RIGI inhibited the proliferation, migration and invasion of colon cancer cells, as well as tumor growth in a nude mouse xenograft model of colon cancer. To investigate the mechanisms of action of DDX58/RIGI in colon cancer, the role of signal transducer and activator of transcription 3 (STAT3)/cystathionineγlyase (CSE) signaling in the up or downregulation of DDX58 was examined. The data demonstrated that DDX58 regulated the STAT3/CSE signaling pathway by interacting with STAT3 and consequently affecting the proliferation of tumor cells in colon cancer. In addition, the RIGI agonist, SB9200, induced proliferation, migration and invasion of human colon cancer. On the whole, the present study demonstrates that DDX58/RIGI affects the proliferation of tumor cells by regulating STAT3/CSE signaling in colon cancer. The findings presented herein suggest that DDX58/RIGI activation may be an effective treatment strategy, and DDX58/RIGI agonists may be potential therapeutic candidates for colon cancer.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Neoplasias del Colon
/
Factor de Transcripción STAT3
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Int J Oncol
Asunto de la revista:
NEOPLASIAS
Año:
2022
Tipo del documento:
Article