ArticleOncogene2020
Activating CCT2 triggers Gli-1 activation during hypoxic condition in colorectal cancer.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 47 citations in OpenAlex.
- CCT2 Promotes Immune Escape in Colorectal Cancer by Regulating the JAK1-STAT3-PD-L1 Axis.Journal of gastroenterology and hepatology · 2026Article
- Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation.Oncology reports · 2026Article
- CRISPR/Cas9 library screening uncovered CCT2 as a critical driver of acquired resistance to EGFR-targeted therapy by stabilizing TMX1 in non-small cell lung cancer.Cell death and differentiation · 2026Article
- CCT7 predicts poor prognosis and correlates with immune infiltration in colonic adenocarcinoma.Journal of molecular histology · 2026Article
- CCT2 Orchestrates Glycolysis and Exosome-Mediated M2 Macrophage Polarization in HCC tumorigenesis.International journal of biological sciences · 2026Article
- Circular RNA CLASP1 modulates the GLI1/SNAIL axis and enhances macrophage polarization in breast cancer.Oncogene · 2025Article
- Histone lactylation drives METTL3 upregulation-mediated RNA m6A modification of CCT2 to hinder CD8Cellular and molecular life sciences : CMLS · 2025Article
- Crosstalk between the circadian clock, intestinal stem cell niche, and epithelial cell fate decision.Genes & diseases · 2025Review
- TRIM38 Suppresses the Progression of Colorectal Cancer via Enhancing CCT6A Ubiquitination to Inhibit the MYC Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Trim21-mediated CCT2 ubiquitination suppresses malignant progression and promotes CD4Cell death & disease · 2024Article
- Article
- CCT6A facilitates lung adenocarcinoma progression and glycolysis via STAT1/HK2 axis.Journal of translational medicine · 2024Article
- Revisiting the chaperonin T-complex protein-1 ring complex in human health and disease: A proteostasis modulator and beyond.Clinical and translational medicine · 2024Review
- CCT2 prevented β-catenin proteasomal degradation to sustain cancer stem cell traits and promote tumor progression in epithelial ovarian cancer.Molecular biology reports · 2024Article
- A hsa_circ_001726 axis regulated by E2F6 contributes to metastasis of hepatocellular carcinoma.BMC cancer · 2024Article
- A potential tumor marker: Chaperonin containing TCP‑1 controls the development of malignant tumors (Review).International journal of oncology · 2023Review
- Profiling neuronal methylome and hydroxymethylome of opioid use disorder in the human orbitofrontal cortex.Nature communications · 2023Article
- THOC3 interacts with YBX1 to promote lung squamous cell carcinoma progression through PFKFB4 mRNA modification.Cell death & disease · 2023Article
- Imputation of single-cell transcriptome data enables the reconstruction of networks predictive of breast cancer metastasis.Computational and structural biotechnology journal · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia, or the deficiency of oxygen, in solid tumors is majorly responsible for the progression of cancer and remains unaffected by chemotherapy, but still requires definitive definition of the hypoxia signaling. Hypoxia disrupts the complete folding of mitochondrial proteins, leading to several diseases. The present study confirms that hypoxia activates the Hedgehog pathway in colorectal cancer (CRC), considering its role in cancer epithelial to mesenchymal transition, migration, and invasion. The activity of hypoxia-mediated Gli-1, a Hedgehog signaling factor in hypoxia, was confirmed by in vitro western blotting, immunofluorescence staining, wound-healing assay, and matrigel invasion assay, as well as by in vivo xenograft models (n = 5 per group). The Gli-1 mechanism in hypoxia was analyzed via mass spectrometry. Hypoxia enhanced the interaction of Gli-1 and T-complex protein 1 subunit beta (CCT2), as observed in the mass spectrometric analysis. We observed that reduction in CCT2 inhibits tumor induction by Gli-1. Ubiquitination-mediated Gli-1 degradation by β-TrCP occurs during incomplete folding of Gli-1 in hypoxia. The human CRC tissues revealed greater CCT2 expression than did the normal colon tissues, indicating that higher CCT2 expression in tumor tissues from CRC patients reduced their survival rate. Moreover, we suggest that CCT2 correlates with Gli-1 expression and is an important determinant of survival in the CRC patients. The results reveal that CCT2 can regulate the folding of Gli-1 in relation to hypoxia in CRC.
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