ArticleOncotarget2014
CUL4A contributes to the biology of basal-like breast tumors through modulation of cell growth and antitumor immune response.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Comprehensive analysis of the Cullin family of genes reveals that CUL7 and CUL9 are the significant prognostic biomarkers in colorectal cancer.American journal of translational research · 2024Article
- LncRNA H19 Impairs Chemo and Radiotherapy in Tumorigenesis.International journal of molecular sciences · 2022Review
- Bothrops Jararaca Snake Venom Modulates Key Cancer-Related Proteins in Breast Tumor Cell Lines.Toxins · 2021Article
- Cullin Ring Ubiquitin Ligases (CRLs) in Cancer: Responses to Ionizing Radiation (IR) Treatment.Frontiers in physiology · 2019Review
- Replication-dependent histone isoforms: a new source of complexity in chromatin structure and function.Nucleic acids research · 2018Review
- Estrogenic regulation of skeletal muscle proteome: a study of premenopausal women and postmenopausal MZ cotwins discordant for hormonal therapy.Aging cell · 2017Article
- CUL4A overexpression as an independent adverse prognosticator in intrahepatic cholangiocarcinoma.BMC cancer · 2017Article
- A new layer of degradation mechanism for PR-Set7/Set8 during cell cycle.Cell cycle (Georgetown, Tex.) · 2016Article
- Genomic profiling of murine mammary tumors identifies potential personalized drug targets for p53-deficient mammary cancers.Disease models & mechanisms · 2016Article
- Cancer stem cells and early stage basal-like breast cancer.World journal of obstetrics and gynecology · 2016Article
- DDA1 promotes stage IIB-IIC colon cancer progression by activating NFκB/CSN2/GSK-3β signaling.Oncotarget · 2016Article
- Cullin 4A (CUL4A), a direct target of miR-9 and miR-137, promotes gastric cancer proliferation and invasion by regulating the Hippo signaling pathway.Oncotarget · 2016Article
- ZYG11A serves as an oncogene in non-small cell lung cancer and influences CCNE1 expression.Oncotarget · 2016Article
- The role and mechanism of CRL4 E3 ubiquitin ligase in cancer and its potential therapy implications.Oncotarget · 2015Review
- Non-coding RNAs derived from an alternatively spliced REST transcript (REST-003) regulate breast cancer invasiveness.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CUL4A E3 ubiquitin ligase is involved in the regulation of many cellular processes and its amplification and/or overexpression has been observed in breast cancer. The 13q34 amplification, which is associated with the basal-like breast cancer subtype, has been proposed as one of the mechanism behind CUL4A up-regulation. However, the specific contribution of CUL4A to the biology of basal-like breast tumors has not yet been elucidated. In this work, by using cellular models of basal phenotype, we show the inhibitory effect of CUL4A silencing in the proliferation and growth of breast cancer cells both, in vitro and in vivo. We also demonstrate the transforming capacity of CUL4A exogenous overexpression in the 184B5 human mammary epithelial cells in vitro. Our results suggest a synergistic effect between CUL4A high levels and the activation of the RAS pathway in the tumorigenesis of basal-like breast cancer tumors. In addition, by using a proteomics approach we have defined novel candidate proteins and pathways that might mediate the oncogenic effect of CUL4A. In particular, we report a putative role of CUL4A in bypassing the immune system in breast cancer through the down-regulation of several molecules involved in the immune surveillance. These findings provide insight into the oncogenic properties of CUL4A in basal-like breast cancer and highlight the therapeutic opportunities to target CUL4A.
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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.