ArticleBioMed research international2021
ICT1 Promotes Osteosarcoma Cell Proliferation and Inhibits Apoptosis via STAT3/BCL-2 Pathway.
Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Evaluating the feasibility of gene replacement strategies to treat MTRFR deficiency.Disease models & mechanisms · 2025Article
- Insights into the Molecular Mechanisms of Bushen Huoxue Decoction in Breast CancerCurrent computer-aided drug design · 2025Article
- Diversity and Similarity of Termination and Ribosome Rescue in Bacterial, Mitochondrial, and Cytoplasmic Translation.Biochemistry. Biokhimiia · 2021Review
- Functional Diversity of Mitochondrial Peptidyl-tRNA Hydrolase ICT1 in Human Cells.Frontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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Abstract
Osteosarcoma (OS) is a familiar malignant bone tumor that occurs mainly in adolescents. Immature colon carcinoma transcript-1 (ICT1) is an important member of the large mitoribosomal subunit in mitochondrial ribosomes, which has been shown to be closely related to tumorigenesis. Its expression and function in OS, however, remained unclear. Here, we showed that ICT1 was significantly upregulated in OS and promoted the growth of OS cells. Mechanistically, ICT1 acted as an oncogene in OS and promoted proliferation and inhibited apoptosis of OS cells through the STAT3/BCL-2 axis. These results reveal a novel insight into the role of the ICT1/STAT3/BCL-2 axis in OS and therefore may represent a novel molecular target for novel treatments.
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