ArticleAmerican journal of cancer research2022
The E3 ubiquitin ligase RBCK1 promotes the invasion and metastasis of hepatocellular carcinoma by destroying the PPARγ/PGC1α complex.
Article in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Vitamin D promotes apoptosis and enhances cisplatin sensitivity in bladder cancer cells by inhibiting the Warburg effect through the AKT/mTOR pathway.BMC urology · 2025Article
- The LUBAC subunit HOIL-1 promotes the progression of HBV-associated hepatocellular carcinoma independently of linear ubiquitination.Experimental & molecular medicine · 2025Article
- Article
- Article
- PRI-724 and IWP-O1 Wnt Signaling Pathway Inhibitors Modulate the Expression of Glycolytic Enzymes in Tongue Cancer Cell Lines.Current issues in molecular biology · 2023Article
- Mechanisms underlying linear ubiquitination and implications in tumorigenesis and drug discovery.Cell communication and signaling : CCS · 2023Review
- SMAR1 inhibits proliferation, EMT and Warburg effect of bladder cancer cells by suppressing the activity of the Wnt/β-catenin signaling pathway.Cell cycle (Georgetown, Tex.) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The disruption of tumour cell metabolism can inhibit tumour metastasis, indicating that aerobic glycolysis is central to tumour development. However, the key factors responsible for mediating aerobic glycolysis in hepatocellular carcinoma (HCC) remain unknown. Here, we observed that RBCK1 expression was significantly upregulated in HCC tissues. Our clinical study revealed that high RBCK1 expression is significantly correlated with poor tumour survival and distant invasion. Functional assays revealed that RBCK1 promotes migration and invasion by enhancing GLUT1-mediated aerobic glycolysis. Furthermore, RBCK1-induced HCC cell migration and aerobic glycolysis via activation of WNT/β-catenin/GLUT1 pathway, which was dependent on the destruction of the PPARγ/PGC1α complex. Mechanistically, RBCK1 promotes PPARγ ubiquitination and degradation, and RBCK1 overexpression enhances the transcriptional activity of WNT/β-catenin, thus to upregulate the expression of GLUT1-mediated aerobic glycolysis in HCC cells. Altogether, our findings identify a mechanism used by HCC cells to survive the nutrient-poor tumour microenvironment and provide insight into the role of RBCK1 in HCC cellular adaptation to metabolic stresses.
Indexed as
Identifiers
35411229PMC8984891W4225817587What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.