ArticleScientific reports2014
UbcH10 overexpression increases carcinogenesis and blocks ALLN susceptibility in colorectal cancer.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 28 citations in OpenAlex.
- UBE2C: a potential therapeutic target and prognostic biomarker for prostate cancer patients.Functional & integrative genomics · 2025Article
- Role of protein degradation systems in colorectal cancer.Cell death discovery · 2024Review
- Ubiquitination-Binding Enzyme 2C is Associated with Cancer Development and Prognosis and is a Potential Therapeutic Target.OncoTargets and therapy · 2024Review
- Ubiquitin‑conjugating enzymes as potential biomarkers and therapeutic targets for digestive system cancers (Review).Oncology reports · 2023Article
- Gatekeepers of the Gut: The Roles of Proteasomes at the Gastrointestinal Barrier.Biomolecules · 2021Review
- CCNI2 plays a promoting role in the progression of colorectal cancer.Cancer medicine · 2021Article
- UBE2C is a Potential Biomarker for Tumorigenesis and Prognosis in Tongue Squamous Cell Carcinoma.Diagnostics (Basel, Switzerland) · 2020Article
- UbcH10 a Major Actor in Cancerogenesis and a Potential Tool for Diagnosis and Therapy.International journal of molecular sciences · 2020Review
- The expression of ubiquitin-conjugating enzyme E2C and KAI1 in ovarian carcinoma and their clinical significance.Medicine · 2019Observational
- Article
- UBE2C promotes rectal carcinoma via miR-381.Cancer biology & therapy · 2018Article
- Forkhead Box M1 positively regulates UBE2C and protects glioma cells from autophagic death.Cell cycle (Georgetown, Tex.) · 2017Article
- UBE2C induces EMT through Wnt/β‑catenin and PI3K/Akt signaling pathways by regulating phosphorylation levels of Aurora-A.International journal of oncology · 2017Article
- The Toxic Effect of ALLN on Primary Rat Retinal Neurons.Neurotoxicity research · 2016Article
- The Spindle Assembly Checkpoint Is Not Essential for Viability of Human Cells with Genetically Lowered APC/C Activity.Cell reports · 2016Article
- High expression of UBE2C is associated with the aggressive progression and poor outcome of malignant glioma.Oncology letters · 2016Article
- Ubiquitin proteasome system research in gastrointestinal cancer.World journal of gastrointestinal oncology · 2016Review
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
Cyclins are essential for cell proliferation, the cell cycle and tumorigenesis in all eukaryotes. UbcH10 regulates the degradation of cyclins in a ubiquitin-dependent manner. Here, we report that UbcH10 is likely involved in tumorigenesis. We found that cancer cells exposed to n-acetyl-leu-leu-norleucinal (ALLN) treatment and UbcH10 depletion exhibit a synergistic therapeutic effect. Abundant expression of UbcH10 drives resistance to ALLN-induced cell death, while cells deficient in UbcH10 were susceptible to ALLN-induced cell death. The depletion of UbcH10 hindered tumorigenesis both in vitro and in vivo, as assessed by colony formation, growth curve, soft agar and xenograft assays. These phenotypes were efficiently rescued through the introduction of recombinant UbcH10. In the UbcH10-deficient cells, alterations in the expression of cyclins led to cell cycle changes and subsequently decreases in tumorigenesis. The tumorigenesis of xenograft tumors from UbcH10-deficient cells treated with ALLN was decreased relative to wild-type cells treated with ALLN in nude mice. On the molecular level, we observed that UbcH10 deficiency enhances the activation of caspase 8 and caspase 3 but not caspase 9 to impair cell viability upon ALLN treatment. Collectively, our results suggest that, as an oncogene, UbcH10 is a potential drug target for the treatment of colorectal cancer.
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.