Affiliation:
1. Department of Gastroenterology, Sixth Affiliated Hospital of Wenzhou Medical University, Lishui People's Hospital, Lishui 323000, China
2. Department of General Practice, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China
3. Department of Gastrointestinal Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing 100142, China
Abstract
Background. Retinoic acid-inducible gene-I (RIG-I) has crucial effects on various cancers, while RIG-I’s detailed roles and mechanism in colorectal cancer (CRC) are uncovered. Methods. qRT-PCR was used to detect the expression of RIG-I in CRC, adjacent nontumor specimens, and five cell lines. CCK-8, colony formation, and flow cytometry assays were conducted to study CRC cell viabilities. Extracellular acidification rates, lactate analysis, and ATP analysis were conducted to study the cell viabilities and glucose metabolism of CRC cells. Western blot is used to determine the proteins of NF-κBp65 in the nucleus and cytoplasm. Results. This study revealed the upregulation of RIG-I in CRC tissues and cells and that high RIG-I expression was correlated with poor prognosis of CRC patients. In addition, silencing RIG-I inhibited cell viability as well as colony formation and promoted cell apoptosis in CRC cells, while RIG-I knockdown suppressed transplanted tumor growth and facilitated apoptosis in nude mice. Moreover, silencing RIG-I inhibited glucose metabolism by decreasing extracellular acidification rate, lactate production, adenosine triphosphate, and content of hypoxia-inducible factor 1α and pyruvate kinase isoform. 2.2-Deoxy-d-glucose, a glycolysis inhibitor, reduced the growth of CRC cells and promoted apoptosis in vitro and in vivo. In addition, RIG-I knockdown decreased NF-κB nuclear translocation. Besides, inhibiting NF-κB effectively eliminated RIG-I overexpression roles in cell viability and glucose metabolism in CRC cells. Conclusion. In summary, this study revealed that RIG-I mediated CRC cell proliferation, apoptosis, and glucose metabolism at least partly by NF-κB signaling pathway.
Funder
Clinical Research Foundation of Zhejiang Medical Association
Subject
Biochemistry (medical),Clinical Biochemistry,Genetics,Molecular Biology,General Medicine
Cited by
4 articles.
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