ArticleCancer science2019
Mitochondrial E3 ubiquitin ligase 1 promotes autophagy flux to suppress the development of clear cell renal cell carcinomas.
Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 24 citations in OpenAlex.
- NCOA7 inhibits renal cancer progression by inducing autophagy and lipid metabolism through V-ATPase interaction.Cell death discovery · 2025Article
- Ubiquitination and De-Ubiquitination in the Synthesis of Cow Milk Fat: Reality and Prospects.Molecules (Basel, Switzerland) · 2024Review
- HIF-2α expression and metabolic signaling require ACSS2 in clear cell renal cell carcinoma.The Journal of clinical investigation · 2024Article
- MFN2 suppresses the accumulation of lipid droplets and the progression of clear cell renal cell carcinoma.Cancer science · 2024Article
- Ginsenoside compound K protects against cerebral ischemia/reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy.Journal of ginseng research · 2023Article
- Autophagy/Mitophagy Regulated by Ubiquitination: A Promising Pathway in Cancer Therapeutics.Cancers · 2023Review
- Review
- Prognostic value of autophagy-related genes based on single-cell RNA-sequencing in colorectal cancer.Frontiers in genetics · 2023Article
- A novel autophagy-related long non-coding RNAs prognostic risk score for clear cell renal cell carcinoma.BMC urology · 2022Article
- Double-stranded RNA-specific adenosine deaminase-knockdown inhibits the proliferation and induces apoptosis of DU145 and PC3 cells by promoting the phosphorylation of H2A.X variant histone.Oncology letters · 2021Article
- miR-30d-5p suppresses proliferation and autophagy by targeting ATG5 in renal cell carcinoma.FEBS open bio · 2021Article
- Beyond glycolysis: Hypoxia signaling as a master regulator of alternative metabolic pathways and the implications in clear cell renal cell carcinoma.Cancer letters · 2020Review
- Article
- Identification of an Autophagy-Related Prognostic Signature for Clear Cell Renal Cell Carcinoma.Frontiers in oncology · 2020Article
- Mitochondrial E3 ubiquitin ligase 1 promotes autophagy flux to suppress the development of clear cell renal cell carcinomas.Cancer science · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Clear cell renal cell carcinoma (ccRCC) is one of the most common malignant tumors in the urinary system. Surgical intervention is the preferred treatment for ccRCC, but targeted biological therapy is required for postoperative recurrent or metastatic ccRCC. Autophagy is an intracellular degradation system for misfolded/aggregated proteins and dysfunctional organelles. Defective autophagy is associated with many diseases. Mul1 is a mitochondrion-associated E3 ubiquitin ligase and involved in the regulation of divergent pathophysiological processes such as mitochondrial dynamics, and thus affects the development of various diseases including cancers. Whether Mul1 regulates ccRCC development and what is the mechanism remain unclear. Histochemical staining and immunoblotting were used to analyze the levels of Mul1 protein in human renal tissues. Statistical analysis of information associated with tissue microarray and The Cancer Genome Atlas (TCGA) database was conducted to show the relationship between Mul1 expression and clinical features and survival of ccRCC patients. Impact of Mul1 on rates of cell growth and migration and autophagy flux were tested in cultured cancer cells. Herein we show that Mul1 promoted autophagy flux to facilitate the degradation of P62-associated protein aggresomes and adipose differentiation-related protein (ADFP)-associated lipid droplets and suppressed the growth and migration of ccRCC cells. Levels of Mul1 protein and mRNA were significantly reduced so that autophagy flux was likely blocked in ccRCC tissues, which is potentially correlated with enhancement of malignancy of ccRCC and impairment of patient survival. Therefore, Mul1 may promote autophagy to suppress the development of ccRCC.
Indexed as
Identifiers
What 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.