ArticleBreast cancer research : BCR2025
CAND1 mediates CUL7-dependent HER2 protein stability to drive breast cancer progression.
Article in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundHER2-positive breast cancer is a prevalent pathological subtype of breast cancer. Resistance to anti-HER2 targeted therapies remains a significant challenge in treatment. Understanding the role of HER2 in breast cancer progression is essential.
methodsThe proteomics analysis was used to explore the regulated proteins in patients with HER2-positive breast cancer. MTS, EdU staininig, flow cytometry and colony formation assays were used to cell proliferation and apoptosis. Protein expressions and interaction of CAND1 and HER2 were clarified by western blot, immunofluorescence and co-immunoprecipitation experiments. In vivo studies using nude mice demonstrated the role of CAND1 in HER2-positive breast cancer cell growth.
resultsAn increase in CAND1 expression, which is associated with poor prognosis in patients with HER2-positive breast cancer. Functionally, CAND1-KD suppresses the growth of HER2-positive breast cancer cells by inducing cell cycle arrest and apoptosis. In vivo, CAND1-KD inhibits tumor growth in xenograft models. Mechanistically, CAND1 expression is positively correlated with HER2 protein levels in breast cancer tissues. CAND1 directly interacts with HER2, stabilizing its protein expression. The E3 ligase CUL7 promotes HER2 ubiquitination and is essential for the interaction between CAND1 and HER2. CAND1-KD enhances CUL7 neddylation, which activates its ligase activity and leads to HER2 ubiquitination. Importantly, HER2 overexpression reverses the proliferation inhibition caused by CAND1 loss both in vitro and in vivo.
conclusionIn summary, this study highlights the critical role of CAND1 in regulating HER2 ubiquitination and suggests a potential therapeutic strategy for patients with HER2-positive breast 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.